#Journal of Cardiac Surgery Case Reports

[killed-by-choice]

“Jayden Roe” (USA ~2024)

The case report of a young girl who died from a chemical abortion was published in the July 2024 edition of the Wisconsin Medical Journal. Except for how she died, very little is known about her. Even her exact age was not specified. She has been given the name “Jayden” here.

Jayden, an adolescent patient, was admitted to the ER for abdominal pain that continuously worsened. She had undergone a mifepristone-misoprostol chemical abortion eight days before. The tests performed in the ER showed retained tissue had been left in Jayden’s uterus, so a suction curettage surgery was performed to remove her dead child’s remains. She did not have a fever and was sent home.

The next day, Jayden was back in the emergency room. She still did not have any fever, but she was tachycardic, hypotensive and suffering from an altered mental state. Her pain was even worse than before. A bedside ultrasound found a large volume of abdominal free fluid. She was taken to the operating room for an exploratory laparotomy.

The laparotomy showed the extent of the infection. Jayden had multiple large-volume ascites, and her bowel was edematous. She was put on a regimen of antibiotics, but the infection raging through her body was already too severe. She was deteriorating quickly.

Even though Jayden was so young, her doctors realized that she needed a hysterectomy to try to control the infection at the source. It would be the third surgery she needed in approximately two days to try to treat her abortion complications. She was brought into the OR where doctors began the surgery to remove her necrotic uterus, but she went into cardiac arrest and died on the operating table.

Jayden’s autopsy results were consistent with toxic shock syndrome. Uterine myonecrosis was identified. Her lab cultures identified the pathogen behind her excruciating death: Clostridium sordellii. Sepsis from C. sordellii and other pathogens is far from unheard of after chemical abortion, even in formerly healthy young patients. It should be noted that although a classic symptom of sepsis is a high fever, patients who contracted sepsis from using abortion pills may have no fever.

Alyona Dixon, Holly Patterson, Oriane Shevin, Sarah Dunn, Manon Jones, Chanelle Bryant, María Del Valle González López, Hoa Thuy “Vivian” Tran, “Wanda Roe,” “Jane Roe” of Canada, “Summer Roe,” “Marcie Roe,” “Crystal Roe,” “Mandy Roe,” “Alina Roe,” “Bridget Roe,” “Chelsea Roe,” “Olivia Roe,” “Carmen Roe,” “Belle Roe,” “Corrie Roe,” “Sabrina Roe” and more were also killed by post-abortion pill sepsis.

[cicaklah]

Pray tell, what is interregnum?

Interregnum is a lot of things, but it mostly contains MORE one man bullshit, such as this journal abstract!

EMBARGOED: FOR INTERNAL STARFLEET MEDICAL PUBLICATION ONLY Starfleet Journal of Interspecies Medicine  McCoy and M’Benga (2260) Case report of improperly broken Vulcan mating bond in psinull human male Patient X is a 26 year old human male in good overall health. Patient Y is a 31 year old male of Vulcan heritage also in good health. Both presented to sickbay with neuropsychic-related trauma at 0300 hours, with X already in late stage organ failure and cardiac arrest and Y in late stage 4 emotional cascade. Patients had an established psychic bond, which was deemed by both to be surplus to requirements. Patient Y performed neuropsychological surgery on himself and patient X in patient Y's quarters using an adapted widely taught method for 'psychic hygiene'. Breaking of the bond was described as 'disproportionately easy' and symptoms took approximately three hours to fully develop. Treatment with cordizine and resus was sufficient to restart patient X's heart, but insufficient to halt the degeneration of his other organ systems. Surgery was performed on two fronts: organ repair and neuro repair, and patient responded well to biobed protocols. Initially patient X stabilised, but later developed several allergies (see forthcoming manuscript). Neuro repair was performed using an outdated and expired NeuroLink2 (expiration date November 2256), retrieved from the personal collection of author b. Despite warnings, the repair was completed successfully. (Paper on impact of out of date medical equipment forthcoming March 2260)

I will never stop.

[nursingwriter]

Heart Disease (CAD: Coronary Artery Disease) Online web site HeartPoint defines Coronary Artery Disease as Coronary artery disease generally refers to the buildup of cholesterol in the inside layers of the arteries. As shown here, this will slowly narrow the flow of blood through the vessel, and the muscle it supplies will not get enough blood. The plaque weakens the wall. As shown in the lower artery, a crack may develop in the plaque and a blood clot may form - this is the mechanism of most heart attacks. Examples and Symptoms of Heart Disease Heart attack is an example of a heart disease that may be sudden or may start as a mild pain. Some of its symptoms are: chest discomfort, in which the patient feels pain in the chest and may feel painful pressure or squeezing in the chest; discomfort in other areas of the upper body, in which the patient feels discomfort and pain in the back, jaw, neck, or arms; shortness of breathing, in which the patient finds it hard to breath caused by pain in the chest; nausea; cold sweat (American Heart Association, 2002). Stroke. According to American Heart Association, some of the symptoms of stroke are: numbness on parts of the body such as arms and legs, sometimes occurs on one side of the body; headache; difficulty in sight; loss of balance of the body; sudden difficulty in comprehension. Cardiac Arrest is an immediate attack and causes a sudden breakdown of the body. Its consequences are: loss of consciousness, abnormal breathing, and sometimes failure of organs and senses to function (American Heart Association, 2002). Risk Factors Heart diseases are caused by several risk factors, either due to heredity or effects of other diseases. HeartPoint lists the following risk factors. Male sex or women who are past their menopause (although women can take hormone replacement therapy). Family history of early CAD in mother, father, sisters or brothers Smoking Diabetes High cholesterol High blood pressure Overweight Sedentary lifestyle, (not exercising enough) Impact of Stress Reports from researches indicate that stress is one of the causes of stroke and heart attacks on patients with CAD. Patients' reaction to stress causes high blood pressure increasing the risk of heart attack, stroke, and cardiac arrest. The issue of Circulation: Journal of the American Heart Association reported that Japanese women who are highly stressed are at double risk of heart disease-related deaths compared to those with low levels of stress (Journal Report, 2002). Prevention Strategies Some of the methods doctors recommend to reduce the risk of heart diseases are: Weight loss - Obesity is among the diseases that is considered a risk factor in heart diseases. Thus, weight loss may lessen fats in the body, minimizing the possibility of developing heart diseases. Smoking Cessation Balanced and Healthy Diet - good eating habits reduces the development of diseases. Treatment Options To recover or prevent heart diseases, doctors usually offer the following options to patients (wral.com, 2003). Change in Lifestyle - this includes a healthy diet, daily exercise, and quitting from vices that cause heart diseases such as smoking and too much intake of alcohols. Medication - this involves treatment of diseases, that cause heart disease, through drugs and medications such as aspirin and nitrates. Surgery - this is the last resort of treatment doctors recommend. This is especially essential in cases where there are internal disorders in the heart and arteries. Bibliography Coronary Artery Disease. HeartPoint. 20 August 2003. http://www.heartpoint.com/coronartdisease.html Heart Attack, Stroke, and Cardiac Arrest Warning Signs. American Heart Association. 20 August 2003. http://www.americanheart.org/presenter.jhtml?identifier=3053#Heart_Attack Heart Attack Symptoms and Warning Signs. HeartInfo.Org. 21 August 2003. http://www.heartinfo.com/search/display.asp?ID=600 Heart Disease Treatment Options. Wral.Com. 22 August 2003. http://www.wral.com/hearthealth/1938335/detail.html Heart Info News. HeartInfo.Org. 22 August 2003. http://www.heartinfo.com/ Read the full article

[jcrmhscasereports]

Retinal and choroidal vascular drop out in a case of severe phenotype of Flammer Syndrome. Rescue of the ischemic-preconditioning mimicking action of endogenous Erythropoietin (EPO) by off-label intra vitreal injection of recombinant human EPO (rhEPO) by Claude Boscher in Journal of Clinical Case Reports Medical Images and Health Sciences

Abstract 

Mediastinal teratoma cysts (cystae mediastinale) are rare incidental findings occurring in approximately 3 to 12 % of all mediastinal cysts (1) Symptoms arise depending on the cyst's specific location (2). This case report describes a 19-year-old female who presented with a mediastinal cyst containing a teratoma. This rare and complex entity was diagnosed through imaging techniques and successfully treated via video-assisted thoracoscopic surgery (VATS). The diagnosis was confirmed by histopathological examination following surgical resection, and the patient's postoperative course was uneventful, with a favourable outcome.

Introduction 

Mediastinal cysts are often discovered incidentally during imaging studies performed for other reasons. These cysts are typically considered congenital anomalies which are usually asymptomatic but can become symptomatic depending on their size and location, potentially causing compression of adjacent cardiac structures ((3). Teratomas are a rare subset of tumors that originate from pluripotent stemcells and can contain elements from all three germ layers (4) teratomas are more commonly found in the gonads (2), their occurrence in the mediastinum, pericardium or myocardium is exceedingly rare ((1) (5). This case report sheds light on the clinical presentation, diagnostic challenges, and successful surgical management of a mediastinal cyst containing a teratoma in a young female patient.

[casereportsjournal]

Journal of Cardiac Surgery Case Reports - Cambridge City Publishers

Cardiovascular Surgery Case Reports Journal publishes Case Reports in Cardiac Surgery, Journal of Cardiac Surgery Case Reports, Cardiac Surgery, Cardiothoracic Surgery Journal etc. Cardiovascular Surgery Journal is a peer-reviewed, open access journal that includes Clinical Images in Cardiac Surgery and surgical treatment of cardiac disease.

Cardiac Surgery Case Reports Journal is a medical journal that focuses on publishing original Cardiovascular Surgery Case Reports Journal and brief communications related to surgical treatments of cardiovascular diseases. It provides a platform for the exchange of practical knowledge and innovative ideas among cardiovascular surgeons, researchers, and other healthcare professionals.

For more information on Cambridge Publishers - Cardiovascular Surgery Case Reports Journal visit our site:- 

[cambridgepublishers]

Cardiac Surgery Case Reports Journal publishes Case Reports in Cardiac Surgery, Journal of Cardiac Surgery Case Reports, Cardiac Surgery, Cardiothoracic Surgery Journal etc. Cardiovascular Surgery Journal is a peer-reviewed, open access journal that includes Clinical Images in Cardiac Surgery and surgical treatment of cardiac disease.

For more information on Cambridge Publishers - Cardiovascular Surgery Case Reports Journal visit our site:- 

https://www.cardiologycasereportsjournal.org/journal/Cardiac-Surgery-Case-Reports-Journal.html

[juniperpublisherscasestudies]

Juniper Publishers- Open Access Journal of Case Studies

Treatment if Pericarditis in an HIV-Infected Patient in a Regional Hospital in Thies (Senegal)

Authored by Bammo M

Summary

Pericarditis is a common and serious cardiovascular disease during HIV infection. In sub-Saharan Africa, tuberculosis is the most common etiology; however, other infectious causes of pericarditis pose a problem of diagnosis and treatment. We report the case of a patient living with HIV 1 for 3 years without ARV treatment who developed a purulent pericarditis treated at regional hospital of Thiès.

We highlight the diagnostic difficulties of this condition in the decentralized zone and the means of treatment of this pathology, fatal if it is not treated early.

Keywords: Purulent pericarditis; HIV infection; Diagnostic difficulties

Introduction

HIV seroprevalence in the Thiès region is 0.3% in 2017. The treatment of PLWAs has been decentralized to the regions and health districts since 2013 with free antiretroviral treatment [1].

a) The immunodepression induced by this virus is at the origin of several affections and/or opportunistic infections responsible for morbidity and mortality, among which cardiac involvement with histological lesions in 60% of cases and clinical expression in 30% of cases.

b) The involvement of the pericardium occupies an important part among these cardiac attacks.

c) The etiological factors of pericarditis vary with the course and magnitude of HIV-induced immune deficiency.

Various causes of pericarditis have been reported in the literature but pericarditis of unidentified (idiopathic) cause can reach 45% of cases [2]. We report the case of an HIV-infected patient who developed a purulent greenish pericarditis of unknown etiology. The objective of this case presentation is to highlight the diagnostic difficulties of this condition in a decentralized environment.

Observation

Mr. Y N is a 26-year-old man, who has sex with a well-known man (MSM), single without children, from the city of Thiès. He presented himself in consultation at the hospital of Thiès October 10, 2016 for a quintessential cough with a notion of hemoptysis of low abundance not objectified. A retrosternal thoracic pain rhythmized by the breathing and a dyspnea with orthopnea type evolving since 15days and exacerbated for a few hours. He also complains of a progressive weight loss of 24kilos in 3years.

For only antecedent, this patient was diagnosed infected with HIV 1, asymptomatic, after a voluntary screening 3 years ago without treatment because He cannot be found. At admission, the patient had a fever at 38.3°C, an impairment of general condition, he was sleepy and cachectic weight 42 kg with BMI: 12.8Kg/m2.

Clinical examination revealed NYA grade 4 dyspnea, tachycardia at 108beats/min and arterial hypotension (BP 100/50mmHg). The heart sounds were muffled. Pericardial friction was not perceptible. There was no paradoxical pulse. Crackling rattles were heard on auscultation at the two pulmonary bases

The rest of the examination found diffuse prurigo and oropharyngeal candidiasis.

The electrocardiogram revealed, in addition to sinus tachycardia, a peripheral low voltage with probable right ventricular hypertrophy, while the chest X-ray showed cardiomegaly and bilateral low-grade pleural effusions.

Complementing the exploration, transthoracic echocardiography confirmed the presence of a pericardial effusion of great abundance without fibrin network. The exploratory puncture aims to produce a purulent yellow-greenish liquid. A percutaneous drainage under xiphoidal under local anesthesia was performed, allowing the evacuation of two liters of greenish-yellow pus free with good tolerance without complications.

The biology revealed an inflammatory syndrome with a CRP of 61.76mg/l and an accelerated sedimentation rate at the first and second hours. There was; microcytic hypochromic anemia at 5.5g/dl, 78.7% neutrophil polynucleosis. Cytobacteriological examination of the pericardial fluid identified 65% of lymphocytes, gram-negative bacilli, but the culture on solid medium was negative. GeneXpert MTB/RIF performed on sputum and pericardial fluid was negative.

As treatment, the patient received an intravenous administration of Ceftriaxone at a rate of 100mg/kg/day; Metronidazole 30mg/kg/day. It was temporarily (3 days) associated with gentamicin (3mg/kg/day) and Prednisone 20mg/day for 5 days. He had also received Furosemide Injection: 40mg/day, Captopril 25mg daily; Enoxaparin 0.4 per day; DLlysine acetylsalicylate 100mg/day. The evolution was marked on day 6 of treatment by a disappearance of cough and dyspnea as well as apyrexia (37°4).

Cardiac echocardiography on day 14 showed a poor pericardial effusion plate insufficient for surgical drainage. The patient was put on antiretroviral therapy and on cotrimoxazole prophylaxis.

The patient was seen six months after discharge in cardiology for signs of late complication; it was stable, with a weight gain of 12kg. Moreover, the M6 ultrasonography showed a quasi-total regression of the pericardial effusion with a slight thickening of the pericardium.

Discussion

This case of purulent pericarditis is singular by its clinical presentation in a PvVIH lost sight of 3 years

Many HIV-infected patients have cardiac involvement [3]. The prevalence of pericardial lesions is regularly reported in all African clinical series: nearly 28% in the Democratic Republic of Congo (DRC) and 35.3% in Congo Brazzaville [2]. In Senegal, already in 1984, D. SOW et al reported a prevalence of purulent pericarditis of 11% in pediatric hospitalized children [4]. I. Thiam found 2.5% of cases of tuberculosis pericarditis with microscopic discovery [5]. Ngouala G. in a study conducted in a decentralized area (Louga) found 3.7% of pediatric cases of tuberculous pericarditis [6].

Pericarditis remains however a serious and rare entity which is almost always fatal because of a late management. The presence of clinical signs and paraclinical examinations allow rapid diagnosis in order to start early treatment [7]. This patient had advanced dyspnea, febrile chest pain on a febrile deterioration of the general condition that had been evolving for 15 days, and effusions indicating delayed diagnosis [3].

The dominant functional symptomatology in the literature is dyspnea of effort and deterioration of the general state. This finding has been made in Africa by several authors [3,8]. Fever is also a reason for frequent consultation. For Cohen, the presence of fever and dyspnea is suggestive of purulent pericarditis or myocarditis [8].

The deafening of heart sounds and tachycardia were the stethoacoustic signs present in our patient and most found in the Niakara and Pio studies, which reported respectively 43.7% and 47.5% of cases [4,8].

The low rate of pericardial friction reported in the literature may be related to the abundance of pericardial effusion [8,9]. He was not present with our patient. Acute pericarditis can be caused by a wide variety of etiologies, which can be infectious or non-infectious [10].

Possible causes include connective tissue disorders, malignancies, radiation, heart lesions, uremia, and infections (including viral, bacterial, and fungal etiologies) [10,11]. In the majority of cases (45 to 80%), infectious pericarditis is of viral origin [11,12].

Bacterial pericarditis is a rare cause of acute pericarditis in the era of modern antibiotics with an incidence of less than 1% [13,14]. The most common living microorganisms involved are Streptococcus sp, Staphylococcus sp, Haemophilus sp and Mycobacterium tuberculosis [15,16].

Pericarditis in a seropositive person, living in Africa in addition, should first look for a tuberculous etiology [3,5,6]. It occurs most often in the early stage of infection, but can also occur in the AIDS stage [3].

No primary infectious focus was found in our patient; the etiological investigation was difficult in our working conditions in the decentralized zone because of the absence of a performing microbiological laboratory, however the favorable evolution under probabilistic antibiotherapy with broad spectrum allowed us to retain the hypothesis of a cause non-specific bacterial.

Predisposing conditions for bacterial pericarditis are immunosuppression, malignant tumors, pre-existing pericardial effusion, alcoholism, uremia, thoracic trauma, cardiac and thoracic surgery, and the insertion or use of catheters for drain the pericardial fluid [15]. This case of pericarditis occurred on HIV-related immunosuppression. The Niakara study in Ouagadougou had a seroprevalence of HIV of 47% out of 79 cases followed for 75 months from 1993 to 1999, reinforcing the work that established a correlation between HIV infection and pericarditis especially in Black Africa [3]. During HIV infection, the occurrence of pericarditis with pericardial effusion is common.

The mechanisms are multiple; pericarditis may be related to viral infection by HIV or other viruses, bacterial or fungal superinfection in an immunocompromised patient or the presence of Kaposi’s lymphoma or sarcoma [3,10,15]. Laboratory assessment may reveal systemic inflammation with leukocytosis and elevated CRP and SV [15]. The chest X-ray usually shows cardiomegaly with an abnormal heart shape. Pulmonary infiltrates, pleural effusion and mediastinal enlargement may also be present [15,16].

The ECG often makes it possible to evoke the diagnosis, especially in its acute form by the Holtzman stages. The signs that we observed at the ECG have no specificity as demonstrated by a piece of literature [9].

In our case, none of the paraclinical examinations were directed to the diagnosis of pericarditis. Echocardiography remains the first-line imaging examination for the diagnosis of pericardial effusion by specifying abundance and location. The abundance of the effusions facilitates the ultrasonography diagnosis of these pericarditis [3,9], as was the case in our patient; he had significant pericardial effusion without cardiac tamponade.

The treatment is based on probabilistic antibiotherapy in the absence of bacteriological data of pericardial fluid and / or blood culture. Surgical drainage is often necessary [8,9]; it allowed our patient to evacuate two liters of greenish yellow pus without complications. Even under treatment, the rate of complications and deaths remains high, with a lethality rate close to 40% secondary to tamponade, pericardial constriction or sepsis [15- 17].

Conclusion

Although rare, purulent pericarditis usually responds to probabilistic treatment provided that a tuberculosis etiology is eliminated even in a health facility with limited means. Early recognition and rapid intervention are essential to the success of the treatment whose etiological research is confronted with daily technical difficulties in a decentralized environment.

For more articles in Open Access Journal of Case Studies please click on: https://juniperpublishers.com/jojcs/index.php

[debofskylaw]

What is accidental death and dismemberment insurance and how does it differ from life insurance?

By Mark DeBofsky

What is an accidental death?

Accidental death insurance is a form of life insurance that pays an indemnity in the event of an “accident” while life insurance is payable merely on account of the death of the insured.  Oddly, most accidental death insurance policies do not include a definition of what is meant by an accident; however, legal precedents have concluded that an “accidental” death is one that is sudden and unexpected.  In addition, when such a death occurs, the deceased must have a subjective expectation of survival and the expectation of survival must be both objectively reasonable and arises under circumstances where death is not substantially certain to result from the insured conduct.  

According to a leading court ruling, “generally, insureds purchase accident insurance for the very purpose of obtaining protection from their own miscalculations and misjudgments.”  Thus, accidental death insurance benefits are payable (unless explicitly excluded) when death results from a drunk driving accident or when the insured engages in dangerous activities such as autoerotic asphyxiation, although court rulings have gone both ways.  

Further, the U.S. Centers for Disease Control publishes a Medical Examiners’ and Coroners’ Handbook on Death Registration and Fetal Death Reporting, which states that coroners or medical examiners list “manner of death” as “accidental” on a death certificate if “there is little or no evidence that the injury or poisoning occurred with intent to harm of cause death.  In essence the fatal outcome was unintentional.”

Is a sudden death due to illness “accidental”?

While no one would intentionally contract a fatal illness, accidental death insurance policies exclude coverage for sudden death which results from an illness such as a heart attack or stroke, or which occurs in the course of undergoing medical treatment.  Death due to COVID or other diseases would also likely be excluded, although front line healthcare and public safety workers who are exposed to the virus in their occupations may have claims for workers’ compensation benefits.  What complicates this issue, and is the source of most litigation over accidental death insurance, are situations where the deceased may have an underlying medical condition that played a role in but did not cause the insured��s death.

Perhaps the best analysis offered in such cases was written in 1893 by future President William Howard Taft while he was serving as a judge on the U.S. Court of Appeals:

“If the deceased suffered death by drowning, no matter what was the cause of his falling into the water, whether disease or a slipping, the drowning, in such case, would be the proximate and sole cause of the disability or death, unless it appeared that death would have been the result, even had there been no water at hand to fall into. The disease would be but the condition; the drowning would be the moving, sole, and proximate cause”.

Insurers have drafted policy language in reaction to such rulings that have made it more difficult for claimants to prevail.  As an example, a recent federal appellate ruling found the deceased’s extensive cardiac history supported the insurer’s conclusion that a heart attack caused him to lose control of his car and die in an ensuing collision, which excluded accidental death coverage.  Other cases have disagreed, though.

Another situation that arises is where an accident leads to a natural death.  An example is a case that we successfully appealed in the U.S. Court of Appeals, Prather v. Sun Life.  There, the decedent injured his Achilles tendon playing basketball, underwent surgery, and died of a pulmonary embolism several days after the surgery.  The court rejected the insurer’s argument that the death was due to natural causes, finding the accidental injury is what led to death.  Remarking on the general rule applicable in such cases, an earlier ruling from the same court observed, “A lay person has a clear if inarticulate understanding of the difference between an accidental death and a death from illness.”

Is an accidental death claim precluded if there is a suspicion of suicide?

While death due to suicide would not be considered accidental, there is a legal presumption against suicide.  Thus, the rule set forth in a court ruling more than a century ago remains applicable:

“In the absence of satisfactory evidence as to the death being accidental or suicidal, the presumption is in favor of the theory of accidental death…” adding “When the dead body of the insured is found under such circumstances, and with such injuries, that the death may have resulted from negligence, accident, or suicide, the presumption is against suicide, as contrary to the general conduct of mankind, a gross moral turpitude not to be presumed in a sane person; and whether it was from one or the other, if there is any evidence upon the point, is for the jury.”

Thus, unless suicidal intent is clear, a death under suspicious circumstances will be viewed as accidental.

What is a “dismemberment” claim

An amputation that results from an accident is also compensable under an accidental death and dismemberment insurance policy.  In cases involving an underlying illness, many courts follow a “substantial contribution” standard.  If injuries resulting from an accident such as a car crash result in an amputation, courts ask whether the illness substantially contributed to the need for the amputation.  Thus, a minor injury such as a cut in the foot that ultimately leads to a leg amputation will likely not be found sufficient to trigger dismemberment coverage if an underlying medical condition such as diabetes predisposed the insured to such a loss.  

What if the deceased was partially at fault in causing an accident?

Many accidental death policies exclude coverage if the death results in the course of the commission of a crime.  But routine traffic infractions, including drunk driving, would generally not trigger such exclusions unless the policy has a specific exclusion applicable to such behavior.  The same rule would apply to an accidental overdose from illicit drug use.  

Should I have both accidental death insurance and life insurance?

Not necessarily.  You should not only have accidental death insurance because statistics compiled by the Centers for Disease Control place the risk of death due to an accident much lower than the overall risk of an early death.  Life insurance is an important component of any financial plan in order to provide familial support in the event of a premature death and buying additional accidental death coverage provides additional support if death or dismemberment results from an accident.  Term life insurance is a relatively inexpensive way to protect against premature death, and because the risk of accidental death is so low, adding such coverage is also relatively inexpensive.  If the goal is to build up savings, though, traditional whole life insurance, while expensive, offers a means of generating savings in addition to insuring against premature death, but does not normally include an additional benefit for accidental death.

About the Author:

Attorney Mark DeBofsky is a member of the firm as well as an adjunct professor of law at University of Illinois-Chicago John Marshall Law School. He is a prolific author who has written many journal articles and has been a regular columnist for the Chicago Daily Law Bulletin since 2004. Mark DeBofsky is also an annual contributor to the ERISA Survey of Federal Circuits published by the American Bar Association and served for many years as a senior editor of Employee Benefits Law published by Bloomberg.

[jcsmicasereports]

Paroxysmal Sympathetic Hyperactivity As A Cause Of Prolonged Icu Stay- Case Report by Arnab Choudhury in Journal of Clinical Case Reports Medical Images and Health Sciences

Abstract

Paroxysmal Sympathetic Hyperactivity (PSH) is commonly described in patients after Traumatic Brain Injury but it can present after an ischemic stroke following a complicated surgery. Usual clinical presentation are tachycardia, tachypnea, hypertension, sweating with seizures and dystonic posturing less likely initial signs. High grade fever and profuse sweating may allude sepsis or epilepsy leading to extraneous administration of anti-epileptics and antibiotics. Suspicion of pheochromocytoma arises in such situations which is ruled out by CECT. Clonidine (α-2 blocker), propranolol (β-blocker) and Baclofen (GABAb agonist) are agents used in treatment. Benzodiazapenes like lorazepam are important part of treatment as discontinuing them can exacerbate PSH attacks. MRI brain with MR angiography usually reveals hyper-intensities on T2/FLAIR in subcortical areas (thalami, cerebellum, crus cerebri) and restricted diffusion with low ADC values. Recurrent PSH episodes can occur due to delay in diagnosing and treatment leading to contractures and difficulty weaning the patient off the ventilator with tracheostomy tube placed. This case presents a scenario in which the delay in diagnosing PSH led to extensive investigations , delay in specific treatment and a prolonged ICU stay of the patient. Mainstay of rehabilitation remains aggressive physiotherapy to improve contractures if any, medications for the autonomic fluctuations and regular follow up.

Keywords : Sympathetic, hyperactivity, paroxysmal, brain, episodes

Introduction

Paroxysmal sympathetic hyperactivity (PSH) is a disorder of autonomic function regulation most commonly observed in patients with acute brain injury. It mostly occurs after traumatic brain injury, but it can also occur after non-traumatic brain diseases such as anoxic-ischemic coma after cardiac arrest, intracranial haemorrhage, and ischemic stroke-[1].

The core clinical features include - tachycardia, tachypnea, hypertension, sweating , hyperthermia and  posturing-[2]. These episodes are mostly triggered by some external stimuli such as pain , movement , and urinary retention . PSH occurs due to diffuse or focal brain injuries that disconnect one or more cerebral centers from the caudal excitatory centers and the disconnection of descending inhibitory pathways causing spinal circuit excitation.

Tonic posturing during  episodes can mimic tonic seizures, and the raised temperature can mimic infection, which can lead to unnecessary investigations, delays in proper management and prolonged ICU stays. Here, we are presenting one such case.

Case Presentation

A 32-year-old woman (gravida 2 and para1) had pain in the lower abdomen at week 31 of gestation for which she was hospitalized and emergency Lower Segment Cesarean Section was performed in view of fetal hypoxia. On the 2nd day post-delivery, she developed multiple episodes of seizures without regaining consciousness in between and was intubated for airway protection.  Brain Magnetic Resonance Imaging(MRI) with angiography suggested posterior circulation ischaemic stroke with bilateral narrow caliber of both vertebral arteries and a left fetal PCA. She was started on antiepileptic drugs and secondary prophylaxis for stroke. She was having high-grade fever and, multiple episodes of profuse sweating per day. Blood counts, cultures, and other markers of infection gave negative Results. She had episodes of tachycardia, tachypnea, hypertension, and sweating associated with fever.

The fever episodes created difficulty in weaning the patient from the ventilator.Therefore, she was started on clonidine and later on, propranolol;-however, these episodes continued to occur. Suspecting pheochromocytoma, abdominal contrast enhanced computed tomography (CECT) was performed, but the results were normal. The patient had recurrent episodes of increase in whole body tone (Fig 1) associated with bilateral lower limb tremors, abnormal posturing along with the above-mentioned episodes of fever. Initially, it was assumed that the rigors were those associated with fever, but later,speculating that the rigors were seizures,- the dosage of herantiepileptic medications were increased, and she was administered triple antiepileptics ( valproic acid , levetiracetam and lorazepam). Her brain EEG showed no epileptiform discharges. Despite receiving triple antiepileptics, she continued to show seizure-like activity. Later, these episodes of fever, tachycardia, tachypnea, hypertension , sweating and increase in body tone occurred simultaneously,- and the diagnosis of paroxysmal sympathetic hyperactivity was made.

The patient was administered clonidine, propranolol, and baclofen. Her episodes of sympathetic hyperactivity were controlled .  Later, her empirical antibiotics were stopped as there was no evidence of infection and fever was explained as a part of sympathetic hyperactivity. Antiepileptic medications were tapered off to only levetiracetam. However, after discontinuing valproate and lorazepam she again started experiencing episodes of sympathetic hyperactivity. Therefore, lorazepam was reintroduced to control her symptoms. Finally, the patient was weaned off ventilator support and shifted to the ward.

Investigations

Blood parameters: TLC - 10,000 /mm3 ,Hb - 12 g/dl , Platelets - 2.8 lac/mm3

Blood culture - no pathogenic organism grown after 48 hrs of aerobic incubation.

Urine culture - sterile

Endotracheal aspirate culture - no pathogenic organism grown after 48 hrs of aerobic incubation.

High vaginal swab culture - normal vaginal flora grown.

Procalcitonin - 0.29 ng/ml

CSF analysis, - Acellular; sugar,-24 mg/dl; protein,-68 mg/dl; culture,-sterile

Dengue IGM,- negative; ICT and peripheral smear for Malaria - negative , Typhidot IGM,- negative; scrub typhus IGM,- negative.

Ultrasound abdomen:- no significant abnormality.

MRI Brain with MR Angiography –The brain stem appeared bulky and showed T2/FLAIR hyperintense signal. Similar areas with T2/ FLAIR hyperintense signal were also seen involving the thalami, right crus cerebri and bilateral inferior cerebellar peduncles. Many of these areas showed restricted diffusion with low Apparent Diffusion Coefficient (ADC) values. The bilateral (right > left) vertebral and distal basilar arteries appeared significantly attenuated in caliber. The right PCA appeared to be significantly attenuated in caliberas compared with fetal origin of the left PCA.

EEG - Generalized cerebral dysfunction; -no epileptiform-discharges.

CECT abdomen - No significant abnormality

Outcome and Follow-up

The episodes of sympathetic hyperactivity resolved, and the patient was shifted to the  ward from the ICU with tracheostomy in room air. She developed contractures owing to persistent decerebrate posturing. Aggressive physiotherapy was administered. In the ward she regained her sensorium and was discharged with a GCS score of E4VTM6 for further follow-up in the OPD.

Discussion

A significant minority of patients who survive acquired brain injury develop sympathetic hyperactivity, which includes episodes of periodic increase in heart rate and blood pressure, sweating, hyperthermia, and motor posturing, often in response to external stimuli, which can last for weeks or more months-[3].Some studies argue that it is common but often unrecognized-[4].Most studies have reported paroxysmal sympathetic hyperactivity after traumatic brain injury. Fewer cases have reported it to be a sequel of brain stroke following prolonged hospital stay.Though commonly seen in TBI, PSH has rarelybeen described in patients with brainstem strokes and anoxic brain injury-[5].PSH may be mistaken for sepsis, which may lead to unnecessary treatment with antibiotics and prolonged hospital stays-[6].Fever is relatively common among patients in the intensive care settings. Although the most obvious and concerning etiology is sepsis, PSH may be the underlying etiology-[7].There are diencephalic structures analogous to the cerebral motor cortex that are capable of producing, when irritated, paroxysmal motor discharges  similar to the focal discharges described as epilepsy-[8].PSA may be camouflaged by epileptic seizures, leading to the unwarranted administration of antiepileptics to the patient. Obstetric patients can present with acute increases in heart rate,-BP and the onset of HELLP syndrome mimicking PSH. Epigastralgia, hypertension, and tachycardia necessitate cesarean section, as in our case, with the subsequent development of HELLP syndrome mimicking PSH.An acute fluid shift from the splanchnic vasculature to the central vasculature may have occurred, causing HELLP syndrome as a result of vasospasm associated with sympathetic hyperactivity. Reporting such cases will facilitate in understanding if the reverse is true, that is, if PSH can mimick as HELLP syndrome-[9,10]. Pregnancy is a risk factor for paroxysmal sympathetic hyperactivity exacerbation, and delivery can result in resolution of the condition-[11].PSH is reclassified as a sympathetic storm rather than an epileptic disorder because of its unresponsiveness to anti-epileptics and the absence of epileptic activity on EEG. [12]it is crucial for clinicians to distinguish this disorder from paroxysmal dystonias. [13,14]Sympathetic storms have been linked to dystonia-like posturing (e.g., PAID, i.e., "paroxysmal autonomic instability with dystonia")[15], Antidopaminergic medications are best avoided to minimize the risk of neuroleptic malignant syndrome, which can potentially mimic PSH (dysautonomia). In contrast to delirium‐associated persistent agitation and picking‐like behaviours, PSH movements are episodic, tend to be provoked by touch, and are uniquely associated with increased sympathetic activityIn the management of this disorder opiates, γ-aminobutyric acid agents, dopaminergic agents, and β-blocker pharmacological agents have been studied. There is a lack of recommendations and comparisons of agents for the management of this disorder.  There is a paucity of recommendations and comparisons of agents for the management of this disorder.  Monotherapy is usually ineffective for the management of paroxysmal sympathetic hyperactivity, and multiple agents with different mechanisms of action should be considered, as in our case .β-blockers have proven to be therapeutic (not as monotherapy) as in our case,α-agonists such as dexmedetomidine have reported therapeautic efficacy in many studies. However, clonidine another α-agonist has shown therapeutic efficacy, as in our case. The effectiveness of physiotherapy in PSH is rarely reported in medical journals; our case strives to provide an example of such therapeutic benefits.

Conclusion

Paroxysmal sympathetic hyperactivity is quite common in patients with brain insult.It can mimic seizures and/or sepsis (due to high grade fever) leading to unnecessary investigations, exposure to higher-grade antibiotics and antiepileptics. Benzodiazepines are beneficial in controlling sympathetic hyperactivity.Non recognition of PSH can lead to difficulty in weaning patients off the ventilator and prolonged hospital stays. Recurrent episodes of sympathetic hyperactivity can lead to significant weight loss and contractures.

[killed-by-choice]

“Carrie Roe,” 24 (USA 2008)

A report from the Department of Obstetrics and Gynecology in Cleveland, Ohio documented a lethal case of multivalvular bacterial endocarditis caused by an abortion. This case study was published in the Obstetrics & Gynecology medical journal.

Carrie was 24, perfectly healthy and had absolutely no history of heart problems. She underwent a “safe and legal” suction curettage abortion at 16 weeks. (Note that the suction method is considered unsuitable at this age because of the size and density of fetal bones.)

Nobody gave Carrie prophylactic antibiotics before the abortion. Ten days later, she came to an emergency room with fever, pain, chills and abdominal tenderness. The hospital suspected a diagnosis of postabortion endometritis with retained fetal tissue. A D&E was scheduled to remove what had been left inside of her. She was placed on antibiotics and underwent the surgery at the hospital one day later.

36 hours after the decaying tissue was removed from her uterus, Carrie was hypoxic and short of breath. After cardiological testing revealed alarming damage, she was rushed into the operating room for emergency heart surgery.

Although she had no pre-existing cardiac conditions, she had developed multivalvular bacterial endocarditis and deteriorated rapidly from infection. During emergency cardiac surgery, an abscess was found inside her heart that measured 2x2 cm and the St. Jude aortic valve was almost completely dehisced from the tissue surrounding it. In her last days of life, she had to undergo multiple heart operations, including a replacement of the aortic valve and surgical debridement of the tricuspid valve.

All attempts to save Carrie’s life failed. She developed disseminated intravascular coagulopathy and went into multi-system organ failure and cardiogenic shock. One day after her emergency heart surgeries, she was brain dead. Her family decided to remove her from life support after neurologic testing confirmed the diagnosis.

Multiple aspects of Carrie’s death were preventable. First, not undergoing the abortion in the first place would have prevented these complications. Secondly, the suction method was inappropriate for 16 weeks and the abortion facility should have known that it would put her at risk for retained body parts. Thirdly, as the medical journal noted, the abortion facility failed to provide timely administration of prophylactic antibiotics.

Carrie’s rapid development of heart infection is strikingly similar to the deaths of 19-year-old Jessie-Maye Barlow in 2012 and Georgette Roe in 1972.

[and-then-there-were-n0ne]

If I were to ask you to picture someone in the throes of a heart attack, you most likely would think of a man in his late middle age, possibly overweight, clutching at his heart in agony. That’s certainly what a Google image search offers up. You’re unlikely to think of a woman: heart disease is a male thing. But this stereotype is misleading. A recent analysis of data from 22 million people from North America, Europe, Asia and Australasia found that women from lower socio-economic backgrounds are 25% more likely to suffer a heart attack than men in the same income bracket. 

Since 1989, cardiovascular disease has been the leading cause of death in US women and, following a heart attack, women are more likely to die than men. This disparity in deaths has been the case since 1984, and young women appear to be particularly at risk: in 2016 the British Medical Journal reported that young women were almost twice as likely as men to die in hospital. This may be in part because doctors aren’t spotting at-risk women: in 2016, the American Heart Association also raised concerns about a number of risk-prediction models ‘commonly used’ in patients with acute coronary syndrome, because they were developed in patient populations that were at least two-thirds male. The performance of these risk-prediction models in women ‘is not well established’. 

Common preventative methods may also not work as well in women. Acetylsalicylic acid (aspirin) has been found to be effective in preventing a first heart attack in men, but a 2005 paper found that it had a ‘nonsignificant’ effect in women aged between forty-five and sixty-five. Prior to this study, the authors noted, there had been ‘few similar data in women’. A more recent study from 2011 found that not only was aspirin ineffective for women, it was potentially harmful ‘in the majority of patients’. Similarly, a 2015 study found that taking a low dose of aspirin every other day ‘is ineffective or harmful in the majority of women in primary prevention’ of cancer or heart disease.

Perhaps the greatest contributor to the numbers of women dying following a heart attack, however, is that their heart attacks are simply being missed by their doctors. Research from the UK has found that women are 50% more likely to be misdiagnosed following a heart attack (rising to almost 60% for some types of heart attack). This is partly because women often don’t have the ‘Hollywood heart attack’ as it’s known in medical circles (chest and leftarm pains). Women (particularly young women) may in fact present without any chest pain at all, but rather with stomach pain, breathlessness, nausea and fatigue. These symptoms are often referred to as ‘atypical’, a designation to which the British Medical Journal took exception in a 2016 article, saying that the term ‘may lead to the underappreciation of risk associated with this presentation’. And under appreciation of the risk may in turn explain why a 2005 US study found that ‘only one in five physicians across multiple specialties was aware that more women than men die from cardiovascular disease each year, and most of these physicians did not rate themselves as effective in treating sex-tailored cardiovascular disease’. 

Atypical or not, for certain types of heart attacks, women (and again especially young women) who present without chest pain are at particular risk of death – which makes it extremely concerning that current NHS England guidelines specify ‘acute cardiac sounding chest pain’ as part of the criteria for a patient being referred for primary percutaneous coronary interventions (PPCI) at one of the country’s specialist twenty-four-hour heart-attack centres. PPCI is an emergency treatment that restores blood flow during a heart attack, and which according to one doctor I spoke to has ‘massively improved survival and outcome’. But this treatment is only carried out at the twenty-four-hour heart-attack centres and, perhaps as a result, 75% of those who receive this treatment are men. The tests doctors use to determine what’s wrong with a patient are also likely contributing to women’s higher death rates following a heart attack. Standard tests like the electrocardiogram or the physical stress test have been found to be less conclusive in women. A 2016 BMJ paper refers to recent work from Edinburgh which showed that the ‘normal’ diagnostic threshold for troponin (a protein released into the blood during heart damage) may be too high for women. And it’s not just about ‘standard’ levels for biomarkers being incorrect in women, we also need to establish new female-specific biomarkers. A biomarker is a biological characteristic (like troponin) whose presence can act as a diagnostic criteria for a specific disease, and a 2014 literature review of sex difference studies suggests that this may be a fruitful area to research. Unfortunately, it concludes that the work done so far is too limited to be able to say whether or not female-specific biomarkers will be found. 

Because women’s heart attacks may not only present differently, but may in fact be mechanically different, the technology we’ve developed to search for problems may not be suitable for female hearts. For example, a heart attack is traditionally diagnosed with an angiogram, which will show where there are obstructed arteries. But women often don’t have obstructed arteries, meaning that the scan won’t show up any abnormalities, and women who turn up at hospital with angina (chest pain) may simply be discharged with a diagnosis of ‘non-specific chest pain’ and told they have no significant disease. Except they do: women with ‘normal’ angiograms have gone on to suffer a heart attack or stroke shortly after being discharged from hospital. Assuming a woman gets lucky and has her heart disease diagnosed, she must then navigate the obstacle course of male-biased treatment: sex differences have not generally been integrated either into ‘received medical wisdom’ or even clinical guidelines. For example, say a man and a woman are both diagnosed with a swollen aorta (the aorta is the main blood vessel that runs from the heart down through the chest and stomach). They are both suffering from an equal level of swelling – but their risk is not the same: the woman has a higher risk of rupture, which carries with it a 65% chance of death. And yet, in Dutch clinical guidelines, the thresholds for surgery don’t differ for each sex.

- Caroline Criado-Pérez’s Invisible Women: Exposing Data Bias in a World Designed for Men

[lupine-publishers-scsoaj]

Why Vasculitis Probably can be Ameliorated with Magnesium and Antagonists of Ceramides and PlateletActivating Factor| Lupine Publishers

Journal of Surgery| Lupine Publishers  

Introduction 

Vasculitis is characterized as an inflammatory disease of the body’s small blood vessels, particularly in the lungs and kidneys [1-4]. Many other organ regions are usually affected which often induces morbidity and mortality [1-4]. Although the exact causes of vasculitis are not known, it appears to be an autoimmune disease even though physical, chemical injuries and infections can result in vasculitis [1-4]. It is classified as a rare disease in the USA because there are only about 200,000 cases. Although numerous treatments have been advocated, there is no known cure or preventative treatment. Vasculitis often leads to difficulties in breathing and renal shut -down. In addition, vasculitis leads to cardiac malfunctions, cardiac failure and strokes. Vasculitis is clearly more common in the aged [1-4]. Recently, we have found that a few patients that were diagnosed with vasculitis appear to have a magnesium deficiency (MgD), particularly in the serum ionized Mg2+fraction [unpublished findings].

Case Report 

Unlike atherosclerosis that takes decades to develop, vasculitis of small and medium sized arterial vessels, as well as microscopic arterioles. venules and capillaries, progresses rapidly, thus producing tissue ischemia via lumen-occlusive intimal hyperplasia and inflammatory syndromes [1-4]. Whether the end result is giant cell arteritis (GCA), polyarteritis nodosa (PAN), Churg- Strauss vasculitis (CSV), Wegner granulomatosis (WG), polymyalgia rheumatica (PR), Behcets disease (BD), or other vascular diseases, invasion of the arterial and microcirculatory walls by macrophages, leukocytes and CD4 T-cells seems to be pivotal [1-4]. In addition, most of these patients appear to demonstrate coagulationopathies. The degrees of luminal stenoses vary from patient to patient. Usually, degradation of the internal elastic laminae (EL) follow suit [1-3]. It has been hypothesized that the latter stenoses are due to concentric growth of the intima which seems to be related to several angiogenic growth factors, e.g., platelet-derived growth factor (PDGF) and vascular endothelial growth factor (VEGF) [4]. What stimulates the production of these growth factors is not completely known but is thought to involve activation of nuclearfactor-KB (NF-kB) in the macrophages and leukocytes [4]. As stated, the macrophages and leukocytes clearly play key roles in the development of vasculitis. They are activated by NF-kB to produce a host of cytokines and chemokines which are needed for tissue remodeling and granuloma formation in development of vasculitis [2,4]. What activates the macrophages and leukocytes to induce production of NF-kB is not known. 

Why Magnesium Deficiency is Most Likely a Key Player in Development of Vasculitis 

While we were routinely investigating the potential role of magnesium deficiency (MgD) in numerous cardiovascular- diseased patients, who presented with coronary arterial diseases, coronary vasospasm, acute myocardial infarctions (AMIs), congestive heart failure , and strokes, we noted that several of these patients had an underlying vasculitis together with significant deficits in serum ionized Mg, but not necessarily total serum Mg levels [5]. More than 50 years ago, two of us found that reduction in the concentration of extracellular free Mg ions (Mg2+ ) resulted in vasospasm of coronary, cerebral, and peripheral arterial vessels; the lower the [Mg2+ ]0, the more the intense the arterial vasospasm [6-13]. In addition, our laboratories found that microscopic blood vessels in skeletal, cutaneous, and cerebral vascular beds of intact rats, mice, rabbits, guinea- pigs, dogs, and piglets exhibited similar phenomena as dietary Mg intake was reduced over three to 12weeks [14,15]. Moreover, vascular reactivity to circulating humoral and hormonal vasoconstrictor agents (i.e., angiotensin II, norepinephrine, serotonin, numerous peptide mediators, etc.) was intensified when [Mg2+ ]0 was reduced; the lower the [Mg2+ ]0 , the greater the humoral and hormonal-induced vasoconstriction [6-10,13]. It is important to note, here, that these agents are often present at increased, circulating levels in cases of vasculitis. It is now clear that all cases of vasculitis are associated with increased levels of various cytokines and chemokines (e.g., IFN-alpha, IL-1-beta, IL-2, IL-8, IL-10, IL-4, IL-17, TNF-alpha, MCP-1, among others) which are pro-inflammatory in nature [1-4]. We have found that rats placed on MgD diets for 21days generate all of these pro-inflammatory cytokines and chemokines in the blood, cardiac tissues and arterial vessels [16,17]. Other investigators have also reported finding many of these cytokines and chemokines in MgD animals [18]. Furthermore, we have found that. These MgD animals generate growth factors similar to those found in patients presenting with various forms of vasculitis [4,5]. All of these cytokines, chemokines, and growth factors, we found in the MgD animals, were associated with microvascular wall remodeling and pathological alterations in the postcapillary venules, resulting in reduced lumen sizes, increased vascular reactivity, and adherence of leukocytes and macrophages on the endothelial cell walls [19-21], thus, in many respects, similar to what is seen in vasculitis. Last, but not least, we have found that the MgD state that we produced in the rats resulted in activation of NF-kB in cardiac, cerebral, and peripheral vascular smooth muscle cells [16-23]. In view of our findings, we believe, collectively, it is difficult to dismiss the probable role of MgD in the etiology and sustenance of a state of inflammation and vasculitis. Thus, we recommend that our hypothesis should be tested in two ways [24-26]: a) Use a Mg2+ -ion selective electrode like those we helped to pioneer [27-31], in order to carefully measure the levels of ionized free Mg; and b) Administer Mg salts, initially, intravenously, then orally, for extended periods of time. 

Low Mg2+ Induces Leukocyte and Macrophage Sticking, Increased Adhesiveness to Venular Endothelial Walls, and Increased Post-Capillary Permeability in The Microcirculation

 Approximately 40 years ago, Ross et al advanced the hypothesis that atherosclerosis is an inflammatory disease brought about by injury to the endothelial surfaces of the macro- and microcirculations [32]. The hypothesis stated that different forms of injury (e.g., ischemic events) will result in numerous dysfunctions in the homeostatic properties of the endothelium, e.g., increases in adhesiveness of macrophages and leukocytes and/or platelets, alteration in the procoagulant properties, formation/release of cytokines/chemokines and growth factors. Usually, inflammation is defined as a response of microcirculatory blood vessels and the tissues they perfuse to infections and damaged tissues which bring cells and host-defense factors/molecules directly from the circulation to all the diverse sites where they are required in order to eliminate/degrade the offending agents [33]. The mediators of the defense mechanisms include white blood cells, macrophages, phagocytic leukocytes, chemokines, antibodies, and complement proteins [33]. The inflammatory process brings these cells and molecules to the damaged or necrotic tissues. During the normal inflammatory process, macrophages, leukocytes, and monocytes migrate across the venous capillary walls through holes in between the endothelial cells due to increases in permeability and move to the site(s) of injury via chemotaxis. This sequence of events is thought to take place in all types of inflammatory events and in developing vasculitis [34]. The normal mediators for these processes to take place are adhesion molecules, cytokines, and chemokines, all of which we have found in patients with different forms of vasculitis and in MgD [5,23]. 

Probable Contributing Roles of Ceramides and Platelet Activating Factor as a Consequence of MgD to Etiology of Vasculitis

 In the late 1990’s, working with proton-nuclear magnetic resonance spectroscopy (1H-NMRS), and arterial vessels exposed to low Mg2+ levels, two of us found an increased synthesis of several sphingolipids (namely, ceramides, sphingosine, and sphingosine-1- phosphate) along with an increased formation of platelet-activating factor (PAF) [35,36]. We and others have reported that many of these sphingolipids (particularly ceramides) and PAF promote vasoconstriction and vasospasm of different types of arterial blood vessels as well as arterioles and muscular venules in the living microcirculation in situ [22-24,26,37-41]. In addition, three of us found that ceramides and PAF cause increases in postcapillary permeability, leukocyte and macrophage adhesion to the endothelial linings of the postcapillary venules, and migration of these latter cell types to the extravascular tissue spaces [41]. What we found, of particular interest, is that vascular smooth muscle cells (of different types), when exposed, in primary cell culture, to low Mg2+ caused a synthesis of both ceramides and PAF, which could be selectively inhibited using specific antagonists of ceramides and PAF [42]. More than 30 years ago, Cunningham and colleagues reported that sera from rheumatoid vasculitis patients contained platelet-releasing activity [43]. Two years later, Warren and his colleagues, using a rat model of immune complex vasculitis, found that a receptor blocker of PAF inhibited an Arthus reaction [44]. Sera taken from patients in our hospitals which had an underling vasculitis (of diverse origins), and lowered serum ionized Mg, demonstrated increased levels of both ceramides and PAF [5]. We do not believe these findings are merely coincidental. It is our contention that low Mg coupled to increased cellular and serum levels of ceramides and PAF are causal agents in many types of vasculitis.

Conclusion 

Although the exact cause(s) of vasculitis is not known, Mg depletion appears to be a presence in different types of vasculitis. When several of our cardiovascular- diseased patients were admitted to our hospitals, a number of them exhibited an underlying vasculitis coupled with an ionized Mg deficiency along with elevated serum levels of ceramides and PAF. Mg-deficient animals, in our labs, exhibited elevated serum and tissue levels of ceramides and PAF which could be reduced/inhibited with specific antagonists of ceramide and PAF synthesis. Elevated dietary levels of Mg also reduced the synthesis of both ceramides and PAF, at least in experimental animals. Experimental animals fed Mg deficient diets exhibited, in-vivo, inflammatory alterations in the microcirculation similar to those patients presenting with different forms of vasculitis (e.g., elevated cytokines, elevated chemokines, elevated adhesion molecules, elevated tissue levels of NF-kB, along with other substances). In view of these new findings from our laboratories, it is our belief that patients exhibiting vasculitis should be treated with oral Mg supplements along with inhibitors of ceramide and PAF synthesis in order to determine if our hypothesis is valid. 

Acknowledgement 

Much of our original investigations were supported, in part, by research grants from The National Heart, Lung and Blood Institute, The National Mental Health Institute, The National Institute on Drug Abuse, and The National Institute on Alcoholism and Alcohol Abuse along with unrestricted research grants from several  pharmaceutical companies. Some of our studies were initiated while two of us (BMA and BTA) were on the faculty of The Albert Einstein College of Medicine. While our original studies were underway, two of our colleagues passed away, namely Professor Lawrence M. Resnick and Anthony Carella. Both of these outstanding scientists will be sorely missed. 

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Peer-Review Journal of Cardiac Surgery Case Reports

The Journal of Cardiac Surgery Case Reports is a scientific publication that focuses on reporting and documenting case studies in the field of cardiac surgery. It provides a platform for healthcare professionals to share their experiences and findings regarding unique or challenging cases they have encountered in their practice. The journal aims to contribute to the scientific knowledge and understanding of cardiac surgery by presenting detailed case reports, including patient demographics, clinical presentations, diagnostic and surgical approaches, and outcome assessments. It serves as a valuable resource for surgeons, researchers, and other healthcare professionals involved in the field of cardiac surgery.

Peer-Review Journal of Cardiac Surgery Case Reports

It aims to enhance knowledge and understanding of complex cardiac surgeries, innovative techniques, and outcomes. The Journal of Cardiac Surgery Case Reports editorial board ensures that high-quality articles are selected for publication, thereby contributing to the advancement of cardiac surgery practices. Contemporary surgical treatment for cardiac disease is the focus of the peer-reviewed, open access Journal of Cardiac Surgery.

Journal of Cardiac Surgery Case Report Topics Such As:

OPCAB Surgery

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Left ventricular restoration surgery

Immunobiology

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These case reports typically include detailed descriptions of patient demographics, presentation, diagnostic workup, surgical techniques employed, and outcomes. By disseminating these case reports, the Journal of Cardiac Surgery Case Reports facilitates communication and collaboration among cardiac surgeons and researchers worldwide.

The rigorous peer-review process ensures that only the most valuable and clinically relevant reports are published in Journal of Cardiac Surgery Case Reports pages. Authors are highly encouraged to submit their manuscripts through the dedicated platform provided by Cambridge City Publishers.

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Authors are requested Journal of Cardiac Surgery Case Reports to submit their manuscript by using Online Manuscript Submission Portal: https://www.cardiologycasereportsjournal.org/useful-link/journal-of-cardiac-surgery-case-reports.html

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Cardiac Surgery Case Reports Journal publishes Case Reports in Cardiac Surgery, Journal of Cardiac Surgery Case Reports, Cardiac Surgery, Cardiothoracic Surgery Journal etc. Cardiovascular Surgery Journal is a peer-reviewed, open access journal that includes Clinical Images in Cardiac Surgery and surgical treatment of cardiac disease.

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Cardiac Surgery Case Reports Journal publishes Case Reports in Cardiac Surgery, Journal of Cardiac Surgery Case Reports, Cardiac Surgery, Cardiothoracic Surgery Journal etc. Cardiovascular Surgery Journal is a peer-reviewed, open access journal that includes Clinical Images in Cardiac Surgery and surgical treatment of cardiac disease.

For more information on Cambridge Publishers - Cardiovascular Surgery Case Reports Journal visit our site:- https://www.cardiologycasereportsjournal.org/journal/Cardiac-Surgery-Case-Reports-Journal.html