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Regardless of the cause, the acute adrenal crisis is characterized by a shock-like condition due to electrolyte deficit with acidosis, vomiting, diarrhea, hemorrhage, and numbness. Death is often caused by hyponatremia, the result of aldosterone deficiency, leading to cerebral and pulmonary edema.
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Learn More »In this chapter, diseases of the adrenal gland and paraganglia that can cause sudden death will be discussed, including the clinical correlation and pattern, as well as the mechanism and presentation of death. The forensic pathologist’s examination is extremely important since providing a cause of death and other findings previously not known can contribute to the improvement of clinical and surgical management of such patients, and help avoid this undesired outcome in other similar cases. Sudden deaths from adrenal diseases are rare compared to other causes, extremely difficult to recognize clinically, and often discovered at autopsy by thorough postmortem investigations. Forensic pathologists have a pivotal role in investigating sudden deaths, as autopsies are often performed. One reason is that in many jurisdictions, death may only be certified by an attending physician if he or she has recently seen the patient and it is clear that their death was caused by a potentially lethal disease. When death cannot be certified by an attending physician, the patient case is referred for medicolegal investigation. Under these circumstances, the role of the forensic pathologist is twofold: to determine the cause and manner of death and initiate a multidisciplinary process in order to prevent further deaths in existing family members (especially in the case of familial diseases) or in other patients suffering from a similar disorder. Lastly, an autopsy is often ordered by a prosecutor if medical malpractice is suspected, especially if the death occurred at a hospital. Coroners and pathologists are frequently presented with unexpected and sudden deaths, which are, unfortunately, not rare. The definition of sudden death suggested by the World Health Organization is a death occurring within 24 h from the onset of symptoms. However, for most clinicians and pathologists, this interval is too long with many regarding sudden death within one hour from the onset of illness [ 1 ]. Cardiovascular, central nervous system and respiratory diseases account for the majority of unexpected natural deaths. Heart diseases are the main cause of sudden death and most investigated. However, in cases of an unexpected death in young and apparently healthy patients, many other medical conditions need to be considered.
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Learn More »At autopsy, decedents who suffered from chronic adrenocortical insufficiency are often slim and cachectic with a brownish skin pigmentation also seen in anorexia nervosa. Generally, pathologic findings at autopsy may include a low combined weight and atrophy making the adrenal glands difficult to detect. For this reason, multiple slides of the fatty tissue surrounding the superior pole of each kidney should be taken for histologic examination. The microscopic appearance of adrenal gland tissue shows atrophy of adrenal cortical cells, and a collapsed vascular reticulin framework (Figures 1 and 2). Only a few sudden deaths due to an endocrine imbalance in an individual previously known to have been treated for adrenocortical insufficiency are found in the literature. A reported case of a 50-year-old man, whose medical history was significant for Addison’s disease, was found dead in a hotel room [3]. Taking into account this man’s circumstances, medical history, and autopsy findings, cause of death was attributed to acute adrenal crisis secondary to gland hypofunction and insufficiency. Adrenocortical insufficiency can be due to many causes including autoimmune gland destruction, infection, and hemorrhage. 2.1. Autoimmune adrenalitis In industrialized countries, adrenal insufficiency is mostly caused by an autoimmune disease that is particularly challenging to evaluate in postmortem investigation as typical macroscopic findings reveal difficult to detect adrenal glands with markedly reduced size [2]. Histologically, in autoimmune adrenalitis, adrenal glands show significant reduction of cortical parenchyma and lymphocytic and plasma cell infiltration (almost exclusively in the cortical region) associated with the destruction of cortical cells. The major difference between Addison’s disease caused by tuberculosis and autoimmune adrenalitis is that in the former, there is the destruction of the whole gland, whereas in the latter, only the cortex is involved. Typically, the dimension of the adrenal glands is markedly reduced and sometimes undetectable. Microscopically, the cortex is generally atrophied and replaced by islands of large eosinophilic cells, but no fibrosis is seen, even though the residual vascular reticulin framework can be observed. Occasionally, there is moderate infiltration, mainly composed by lymphocytes, with some involvement of the medulla that is otherwise normal. Inflammation is often accompanied by fibrosis [4]. Histologic features seen in autoimmune adrenalitis include the enlargement of surviving cells that also show nuclear atypia, probably due to prolonged ACTH stimulation [2]. There are a few cases describing autoimmune adrenalitis as a cause of sudden death in the literature. In one case report, a 12-year-old girl hospitalized following a 2-day history of recurrent vomiting was given the misdiagnosis of diabetic ketoacidosis [5]. She died shortly after hospitalization. The diagnosis of autoimmune Addison’s disease was rendered at autopsy based on histology. Microscopic examination revealed depletion and atrophy of the adrenal cortex with enlargement, eosinophilia of surviving cortical cells, and prominent round cell infiltrates composed mostly of lymphocytes. In addition, there was mild chronic lymphocytic thyroiditis. Other organs were unremarkable except for marked pulmonary congestion and edema with early basal pneumonic changes and cerebral edema. Undeniably, histopathology is essential for the diagnosis of autoimmune adrenalitis, and examination of postmortem blood, particularly of serum cortisol levels, should be included in the investigation. The availability of appropriately stored antemortem serum samples is of great importance, and cortisol is sufficiently stable in postmortem blood [6]. Levels of cortisol, 17-hydroxycorticosterone, aldosterone, and dehydroepiandrosterone in postmortem serum from femoral blood and urine (in combination with other biochemical investigation) allow for the differentiation between ketoacidosis and adrenocortical insufficiency [7]. An additional examination for adrenal autoantibodies on postmortem serum can be conducted [2]. 2.2. Tuberculosis and other infections involving adrenal glands About 10% of Addison’s disease cases have an infectious etiology [8]. HIV/AIDS and opportunistic infections such as cytomegalovirus are the most commonly cited causes, following tuberculosis. Currently, adrenal tuberculosis has generally considered a disease of immigrants from endemic areas, immunocompromised or destitute individuals. In the past, tuberculosis was the most common cause of adrenocortical insufficiency and remains the primary cause in the developing countries where it accounts for about 20–30% of cases of Addison’s disease. Various fungi including Cryptococcus, Histoplasma, Coccidioides , and Paracoccidioides also infect the adrenal glands as reported in several published case reports. It is well known that Mycobacterium tuberculosis complex spreads to the adrenal glands hematogenously. Clinical manifestations may take 3 years to become apparent, and asymptomatic infection is not uncommon [8]. The only case report, to the authors’ knowledge, of sudden death due to isolated adrenal tuberculosis was reported in 1985 [9]. The patient with a history of a disseminated carcinoma of the prostate presented with normal blood pressure, lack of skin pigmentation, and normal electrolytes. He died suddenly after being admitted to a hospital for investigation of pleural thickening. The autopsy revealed that his adrenal glands were both completely replaced by caseous material containing acid-fast bacilli. There was no evidence of tuberculosis in any other organs. Another important issue regarding the adrenal glands concerns HIV infection. Apart from direct infection, opportunistic infections and antiretroviral medications also have a significant effect on the adrenal glands. Adrenal insufficiency is prevalent in 17% of patients admitted with AIDS [10]. In a forensic context, when dealing with an unexpected death in a subject previously known as having HIV, adrenal insufficiency should be considered and properly investigated. The histopathology and morphologic assessment of the adrenal glands were investigated in 128 autopsied patients who died from AIDS [11]. Interestingly, alteration of the adrenal glands was observed in 99.2% of these decedents with various patterns of disease and different pathogens. Inflammatory infiltrates, mostly with a predominance of mononuclear cells, were observed in 99.2% of the cases. The medulla was almost always involved. Fibrosis, necrosis, neoplasia, and hemorrhage were also detected. Human cytomegalovirus (CMV) has been frequently identified as a cause of adrenal insufficiency, especially in patients with HIV/AIDS. In one report, CMV-infected normal human adrenocortical cells and induced cytopathic changes [12]. CMV also acts as an inducer of steroidogenesis, which may explain the discordance between the high rates of CMV adrenalitis in immunosuppressed patients in autopsy studies and the relatively rare diagnosis of adrenal insufficiency antemortem. Interestingly, while adrenalitis may be the sole manifestation, the disease is usually disseminated. CMV typically affects the cortex-medulla junction [11]. Many other rare infections can affect the adrenal glands. Addisonian crisis has been reported in patients afflicted with such pathogens as: histoplasma capsulatum (commonly in HIV patients with clinical manifestation similar to tuberculosis), paracoccidiomycosis (endemic in several South American countries where adrenal insufficiency has been reported in 2.9–48.2% of patients), viruses (herpes simplex, Epstein Barr, CMV), and, very rarely, other bacteria and parasites [8].
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