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Adrenalectomy
Published in Mark Davenport, James D. Geiger, Nigel J. Hall, Steven S. Rothenberg, Operative Pediatric Surgery, 2020
Mikael Petrosyan, Timothy D. Kane
Development of the adrenal gland begins between 3 and 4 weeks of gestation and cephalad to the developing mesonephros. At this point, the gonadal ridge has yet to form, and there is no distinction between adrenal and gonadal tissue. By 5–6 weeks, however, steroidogenic gonadal cells begin their caudal migration, while the cells that will eventually comprise the zona reticularis migrate dorsally into the retroperitoneum. Over the next several weeks, there is a rapid enlargement of the inner cortex to form the fetal zone (the outer subcapsular rim remains as the definitive zone) and, simultaneously, migrating cells of the neuroectoderm also follow trophic signals to populate the adrenal medulla. These cells will subsequently be responsible for producing and storing catecholamines. The fetal adrenal gland is proportionally much larger than that in the adult. At 8 weeks’ gestation, the adrenals are larger than the kidney, and at term, they are approximately one-third the size of the kidney, with the fetal cortex comprising most of that mass. Within several days of birth, the fetal cortex begins rapid involution and decreases to half the immediate postnatal size at 1 month and one-eighth of its size by 1 year. During this time, the medulla begins a slow period of growth. The relative size of the neonatal adrenal gland is thought to contribute to perinatal adrenal hemorrhage (reported incidence three in 100 000 live births). Occasionally, adrenal hemorrhage may lead to exsanguination and death, or present with an abdominal mass, anemia, or scrotal hematoma.
“Primary” Anti-Phospholipid Syndrome
Published in E. Nigel Harris, Thomas Exner, Graham R. V. Hughes, Ronald A. Asherson, Phospholipid-Binding Antibodies, 2020
Several patients conforming to a PAPS who have developed Addison’s disease have now appeared in the literature.55-57 Antibodies to adrenal tissue have been absent in these patients and in most has been preceded by recurrent DVTs. Vascular occlusions of the hypoadrenalism have been demonstrated in the adrenal vasculature in some of this interesting group of patients, it seems likely that this is the underlying pathogenetic mechanism for the development of this complication. Adrenal hemorrhage in patients on long term anticoagulation therapy may be another pathogenetic mechanism.
Natural Deaths
Published in John M. Wayne, Cynthia A. Schandl, S. Erin Presnell, Forensic Pathology Review, 2017
John M. Wayne, Cynthia A. Schandl, S. Erin Presnell
Answer E is correct. The compendium of findings makes sepsis the most likely cause of death. Diffuse intravascular coagulation (DIC) may be seen in sepsis, neurotrauma, malignancy, and several other conditions, and of note, is a possible finding in heat stroke, which is another key differential diagnosis in this case. The finding of bilateral adrenal gland hemorrhage can be due to any cause of DIC. When due to sepsis, the finding may be termed Waterhouse–Friderichsen syndrome. Any cause of bilateral adrenal hemorrhage may lead to adrenal dysfunction or crisis with up to 50% mortality when due to sepsis. Thus, the finding at autopsy may be of paramount importance in the determination of the cause of death (also see Tormos LT and Schandl CA. The significance of adrenal hemorrhage: Undiagnosed Waterhouse–Friderichsen syndrome, a case series. J Forensic Sci 2013, 58[4]: 1071–4).
Flank pain in the third trimester as a clue to diagnose spontaneous adrenal hemorrhage
Published in Baylor University Medical Center Proceedings, 2022
Busara Songtanin, Nicole Welch, Kenneth Nugent, Anupa Patel
Spontaneous adrenal hemorrhage is a very rare condition that requires prompt diagnosis and treatment. It often presents with nonspecific signs and symptoms, which makes a high index of suspicion critical for the rapid diagnosis of this potentially fatal condition. The most common causes of adrenal hemorrhage are infection and sepsis. However, trauma, anticoagulant use, autoimmune diseases, and pregnancy are also known causes.1 The exact pathophysiology is unknown, but speculation has produced several theories.2 The adrenal glands have a rich vascular supply. Since pregnancy is a stress on the body, the secretion of ACTH can lead to adrenal hypertrophy with an increased vascular supply, thus increasing the risk of venous congestion, which may ultimately lead to hemorrhage.1,2
Using microwave thermal ablation to develop a subtotal, cortical-sparing approach to the management of primary aldosteronism
Published in International Journal of Hyperthermia, 2019
Padraig T. Donlon, Hojjatollah Fallahi, Warren L. Beard, Atif Shahzad, Lindsay Heflin, Whitney Cox, Brooke Bloomberg, James D. Lillich, Chanran K. Ganta, Gerard J. O’Sullivan, Giuseppe Ruvio, Paula M. O’Shea, Martin O’Halloran, Punit Prakash, Michael Conall Dennedy
Our probe design and choice of MTA was specifically chosen to address the challenges and limitations of prior clinical studies which have used adrenal RFA to treat benign functioning adenomas [13]. Previous investigators ablated visible APAs by applying pulsed RFA, applied over 15–20 min, at doses sufficient to induce global adrenal necrosis without specific regard for preserving normally functioning tissue [13,24–26]. When designing our approach to adrenal ablation, we attributed equal importance to preservation of tissue which was not selected for ablation, in addition to subtotal destruction of selected tissue. Our MTA system was evaluated in simulated models and a side-firing applicator probe was chosen to provide a lateral non-penetrative approach, positioning the probe between the adrenal and the peri-adrenal fat [15,16,27]. The focal spot size for the selected power/time combinations was well matched to the target and microwave energy was delivered at low doses (45 W and 70 W) for a shorter time period (60 s vs. 15 min) than described in RFA studies [12–14]. The choice of a non-penetrative approach was important to avoid the risk of adrenal hemorrhage, given the fragility of the adrenal gland [28]. Additionally, placing the probe on the surface of the gland, rather than penetrating the gland, facilitated preferential ablation of the subcapsular cortex, while minimizing damage to the medulla, deeper within the gland.
Bilateral adrenal hemorrhage revealed antiphospholipid syndrome in a male patient: benefit from comprehensive treatment
Published in Current Medical Research and Opinion, 2018
Junqing Xu, Qin Zhou, Nihong Jiang, Zhenming Liu, Hui Gao, Yanbin Sui, Riming Liu, Pingtao Liu, Yajuan Cui
Given the presence of adrenal hemorrhage in this patient, subsequent evaluation was performed. Coagulation profile work-up revealed a normal prothrombin time and prolonged activated thromboplastin time (APTT) of 95.1 s (normal = 23.0 ∼ 35.0 s), which can’t correct with the plasma transfusion, indicating the presence of a circulating anticoagulant. Subsequent laboratory studies revealed a positive anticardiolipin antibody of the IgM isotype (aCL-IgM) and a mildly elevated lupus anticoagulant (LA) of 76.2 s (normal = 30.0 ∼ 41.0 s). The aCL of the IgG isotype (aCL-IgG) (normal negative) and anti-β2-glycoprotein I (β2-GPI) were negative (normal negative). Additionally, anti-nuclear antibodies (ANA) were 1:160 spot positive (normal = 1:80 negative) and anti-double-stranded DNA antibodies (dsDNA) were 120 IU/ml (normal = 0 ∼ 100 IU/ml), together with leukopenia of 2.36 × 109/L, thrombocytopenia of 81 × 109/L, and hypocomplementemia of C3 0.594 g/L (normal = 0.900–1.800 g/L), C4 < 0.063 g/L (normal = 0.100–0.400 g/L), CH50 = 14.0 U/ml (normal = 23.0–46.0 U/ml). Thus, he was diagnosed of APS secondary to SLE with adrenal hemorrhage, which led to adrenal insufficiency.