Decompensation Of Organs Research Articles

Diagnosis dan Tata Laksana <i>Thyroid Storm</i> yang Dipicu oleh Perikarditis Akut

Thyroid storm is a life-threatening condition that requires prompt diagnosis and emergency treatment. This condition manifests as multiple organ decompensation characterized by loss of consciousness, high fever, heart failure, diarrhea,and jaundice. We report a case of a 51-year-old man with a chief complaint of fever that has been felt since the night before admission. Body temperature was up to 38°C and started while he was resting. Patient also reported dry, intense cough, since five days ago, accompanied with shortness of breath when lying down. The patient also felt palpitations sincethe previous night and still felt until the morning of admission, and did not improve with rest. The patient was diagnosed by observation of suspension shock due to cardiogenic shock, suspect Graves’ disease (thyroid storm), ADHF profileB et causa suspect CAD, AF RVR, type 2 DM, myofascial pain syndrome with differential diagnosis: headache related toinfection, hyponatremia chronic asymptomatic hypoosmolar hypervolemic et causa suspect dilution, hypoalbuminemia etcausa suspect chronic inflammation, and upper respiratory tract infection. Thyroid storm cases require a multidisciplinaryapproach in terms of diagnosis and therapy. In this case, the patient is referred to the internal medicine, cardiac, andneurology departments.

Thyroid storm in a postpartum and uncontrolled graves' disease patient: the challenges of accurate and multidisciplinary disease management

Background: Graves' disease is an immune system disorder that results in the overproduction of thyroid hormones (hyperthyroidism). Although pregnancy hyperthyroidism is a relatively uncommon, thyroid crisis is a medical emergency caused by hyperthyroidism exacerbation with symptoms of organ decompensation in one or more organs. Therefore, managing this disease in pregnant women is critical as well as the safety of using antithyroid drugs for pregnant women and the foetus. Case presentation: A 26-year-old woman presented to the Dr Soetomo General Academic Hospital Surabaya, Indonesia with complaints of shortness of breath that had worsened one hour before the admission as well as sudden fever, diarrheal, anxiety, and decreased consciousness. The patient had hyperthyroidism for three years, and the controls were inconsistent. The patient was diagnosed with P1101 postpartum day 1, thyrotoxicosis due to Graves' disease, thyroid crisis, hypertension, microcytic hypochromic anemia, hypoglycemia, hypoalbuminemia, keratitis, and lagophthalmos. The patient was treated with supportive therapy with an oxygen mask 8 liters per minute (lpm), intravenous fluids, and antipyretic acetaminophen 500 mg every 8 hours. Propylthiouracil 400 mg loading dose followed by maintenance 6x100 mg, 8 drops of Lugol's solution after propylthiouracil administration, intravenous (IV) dexamethasone 2 mg every 6 hours, and oral propranolol 20 mg every 6 hours. The patient was discharged from the hospital after presented favorable improvement. Conclusion: This case demonstrates that the stage of the disease determines the management of Grave's disease during pregnancy, and that multidisciplinary involvement could improve the success and reduce the patient mortality.

THROMBOTIC MICROANGIOPATHY: DIAGNOSTIC CHALLENGES IN THE PRIMARY MULTIPLE NEOPLASM INVOLVEMENT WITH PREVALENT METASTASIS WITH GRANULOMATOSIS INFLAMMATORY FOCUSES.

Patient, who died during the hospital stay, had hemoblastosis and syphilis in the reported medical history. While the patient was examined doctors suspected the presence of malignancy with unknown primary localization with multiple metastatic injuries with clinical and laboratory TTP signs (hemorrhagic syndrome, thrombocytopenia, shystocytosis, and non-immune hemolytic anemia). Despite treatment, the general patient's condition progressively worsens with increasing multiple organ decompensation signs. In the final stage of the disease course, after heart arrest and the appearance of clinical death signs CPR measures were performed according to complete guidance, but CRP had no positive effect. Biological death was constated. Considering the criteria of the diagnostic clinical and laboratory dyad (thrombocytopenia and microangiopathic hemolytic anemia), the data of the patholog¬ical examination (multiple metastatic lesions, inflammatory process, tumor intoxication, thrombosis), the combination of manifestations of chronic myeloid leukemia, prostate cancer with multiple metastases, tertiary syphilis served as a condition for the initiation of TTP, which was of decisive importance in the development of the patient's death.

Ultrastructural Changes of Blood Cells in Children with Generalized Purulent Peritonitis: A Cross-Sectional and Prospective Study.

In conditions of abdominal sepsis with indications of first- or second-stage shock, blood cells undergo significant ultrastructural changes that cause impaired gas exchange, changes in reactivity, and decompensation of organs and systems functions. This paper presents a cross-sectional prospective study aimed at researching the ultrastructure of blood cells in children experiencing abdominal septic shock against the background of generalized purulent peritonitis of appendicular origin. This study was conducted with 15 children aged 6–12 who were undergoing treatment for generalized appendicular purulent peritonitis, with first- or second-stage abdominal septic shock, in emergency care. The changes in the ultrastructure of erythrocytes did not correspond to changes characteristic of eryptosis, which confirms their occurrence under the influence of such pathogenic factors as intoxication, metabolic, water–electrolyte balance, and acid–base disorders. Ultrastructural changes of granulocytes indicate their hyperactivation, which leads to the exhaustion of membrane synthetic resources, membrane destruction, ineffective expenditure of bactericidal factors on substrates that are not subject to destruction. In lymphocytes, disorganization of the nuclear membrane and intracellular membranes, uneven distribution of chromatin, the hypertrophied Golgi apparatus, and a large number of young mitochondria, lysosomes, ribosomes, vesicles manifesting the disruption of metabolism, stress and decompensation of energy supply and protein synthesis systems, have been demonstrated. In conditions of abdominal sepsis with indications of first- or second-stage shock, blood cells undergo substantial ultrastructural changes causing gas exchange disruption, changes in reactivity, as well as decompensation of organs and system functioning.

TRPV1 alterations in urinary bladder dysfunction in a rat model of STZ-induced diabetes

AimsMore than half of diabetic patients experience voiding disorder termed diabetic urinary bladder dysfunction (DBD). Here we have investigated how the alterations in transient receptor potential vanilloid 1 (TRPV1) ion channel expressed in bladder-innervating afferents may contribute to DBD pathogenesis. Main methodsThe rat model of streptozotocin (STZ)-induced diabetes was used. The functional profile of TRPV1 in retrogradely labeled afferent, bladder-innervating dorsal root ganglia (DRG) neurons was examined using patch clamp. The level of TRPV1 transcripts in DRG was assessed with qRT-PCR. TRPV1-dependent component of detrusor smooth muscle (DSM) contractions was studied with muscle strip tensiometry. Key findingsTRPV1-mediated current (ITRPV1) was increased in diabetic animals vs. controls by 42%. The expression of Trpv1 gene was found to be 63% higher in STZ-treated rats compared to controls, consistent with the respective electrophysiological data. Surprisingly, capsaicin-induced contractions of DSM were found to be 3-to-10-fold weaker in diabetic group depending on concentration of the agonist (100nM to 10μM). SignificanceOur findings suggest the dual role of TRPV1 in DBD. On the one hand, the increase of its functional expression may enhance micturition reflex arc functioning. On the other hand, at the local level, the decrease of TRPV1-dependent contractions may contribute to organ decompensation.

Двадцатилетний опыт в хирургическом лечении «гигантских» аневризм восходящей аорты

Giant ascending aortic aneurysm is one of the worst lesions of the cardiovascular system. Timely surgical treatment provides the only chance to prolong the lives of such patients. Life expectancy without surgery in these patients is minimal; they die from a ruptured aneurysm or decompensation of organs and systems. In this paper, based on two decades' experience of treating patients with giant aneurysms of ascending aorta and aortic arch in B.V. Petrovsky National Research Center of Surgery we have assessed evaluated immediate results of surgery and proposed measures for prevention of possible complications. Out of 53 patients with giant. ascending aortic aneurysms spontaneous rupture after sternotomy or opening of the pericardium occurred in 5 cases. Overall hospital mortality was 1.9%. Our results indicate that with the right tactics surgical repair of giant ascending aortic aneurysms can be performed with a low mortality. Preliminary cardiopulmonary bypass with peripheral cannulation and cooling prior to sternotomy for the possibility of circulatory arrest is a prerequisite of the prevention of fatal massive hemorrhage.

MicroRNA therapy for the failing heart.

Heart failure (HF) may result from diverse pathological processes leading to progressive organ decompensation. Improper functionality of the calcium-handling machinery is a frequent component of the pathobiology underlying this debilitating process. Case in point, loss of intracellular calcium homeostasis because of decreased function of sarco/endoplasmic reticulum Ca2+-ATPase 2a (SERCA2a) is characteristic of HF, and restoration of SERCA2a function through gene therapy results in improved cardiac performance.1 MicroRNAs (miRNAs) constitute a new family of fine-tuning molecules involved in tight regulation of physiological and pathological processes. In fact, the identity and the level of miRNAs expressed at the systemic and organ levels change with disease. Wahlquist et al2 hypothesize that miRNAs capable of repressing contractility might be involved in HF and could, therefore, be used as therapeutic targets. Specifically, the authors focus their efforts on miRNAs involved in calcium dynamics regulation. To search for miRNAs capable of downregulating SERCA2a, a whole-genome collection of miRNAs was tested on Human Embryonic Kidney 293 cells cotransfected with an enhanced green fluorescent protein reporter fused to the 3′ untranslated region of the SERCA2A gene, enabling functional detection of miRNAs capable of decreasing SERCA2a through a fluorescence (enhanced green …

Cell therapy for cardiac repair—lessons from clinical trials

The global impetus to identify curative therapies has been fuelled by the unmet needs of patients in the context of a growing heart failure pandemic. To date, regeneration trials in patients with cardiovascular disease have used stem-cell-based therapy in the period immediately after myocardial injury, in an attempt to halt progression towards ischaemic cardiomyopathy, or in the setting of congestive heart failure, to target the disease process and prevent organ decompensation. Worldwide, several thousand patients have now been treated using autologous cell-based therapy; the safety and feasibility of this approach has been established, pitfalls have been identified, and optimization procedures envisioned. Furthermore, the initiation of phase III trials to further validate the therapeutic value of cell-based regenerative medicine and address the barriers to successful clinical implementation has led to resurgence in the enthusiasm for such treatments among patients and health-care providers. In particular, poor definition of cell types used, diversity in cell-handling procedures, and functional variability intrinsic to autologously-derived cells have been identified as the main factors limiting adoption of cell-based therapies. In this Review, we summarize the experience obtained from trials of 'first-generation' cell-based therapy, and emphasize the advances in the purification and lineage specification of stem cells that have enabled the development of 'next-generation' stem-cell-based therapies targeting cardiovascular disease.

Thyroid Storm

Thyroid storm, an endocrine emergency first described in 1926, remains a diagnostic and therapeutic challenge. No laboratory abnormalities are specific to thyroid storm, and the available scoring system is based on the clinical criteria. The exact mechanisms underlying the development of thyroid storm from uncomplicated hyperthyroidism are not well understood. A heightened response to thyroid hormone is often incriminated along with increased or abrupt availability of free hormones. Patients exhibit exaggerated signs and symptoms of hyperthyroidism and varying degrees of organ decompensation. Treatment should be initiated promptly targeting all steps of thyroid hormone formation, release, and action. Patients who fail medical therapy should be treated with therapeutic plasma exchange or thyroidectomy. The mortality of thyroid storm is currently reported at 10%. Patients who have survived thyroid storm should receive definite therapy for their underlying hyperthyroidism to avoid any recurrence of this potentially fatal condition.

Induced pluripotent stem cell intervention rescues ventricular wall motion disparity, achieving biological cardiac resynchronization post‐infarction

Dyssynchronous myocardial motion aggravates cardiac pump function. Cardiac resynchronization using pacing devices is a standard-of-care in the management of heart failure. Post-infarction, however, scar tissue formation impedes the efficacy of device-based therapy. The present study tests a regenerative approach aimed at targeting the origin of abnormal motion to prevent dyssynchronous organ failure. Induced pluripotent stem (iPS) cells harbour a reparative potential, and were here bioengineered from somatic fibroblasts reprogrammed with the stemness factors OCT3/4, SOX2, KLF4, and c-MYC. In a murine infarction model, within 30 min of coronary ligation, iPS cells were delivered to mapped infarcted areas. Focal deformation and dysfunction underlying progressive heart failure was resolved prospectively using speckle-tracking imaging. Tracked at high temporal and spatial resolution, regional iPS cell transplantation restored, within 10 days post-infarction, the contractility of targeted infarcted foci and nullified conduction delay in adjacent non-infarcted regions. Local iPS cell therapy, but not delivery of parental fibroblasts or vehicle, prevented or normalized abnormal strain patterns correcting the decrease in peak strain, disparity of time-to-peak strain, and pathological systolic stretch. Focal benefit of iPS cell intervention translated into improved left ventricular conduction and contractility, reduced scar, and reversal of structural remodelling, protecting from organ decompensation. Thus, in ischaemic cardiomyopathy, targeted iPS cell transplantation synchronized failing ventricles, offering a regenerative strategy to achieve biological resynchronization.

Amyloid and the GI tract

Amyloidosis is characterized by the extracellular deposition of an abnormal fibrillar protein, which disrupts tissue structure and function. Amyloid may be localized to a single organ, such as the GI tract, or be systemic where the amyloid type is defined by the respective fibril precursor protein. Among patients with systemic amyloidosis, histological involvement of the gastrointestinal (GI) tract is very common but often subclinical. The presence and pattern of GI symptoms varies substantially, not only between the different amyloid types but also within them. GI presentations are frequently nonspecific and include macroglossia, dyspepsia, hemorrhage, a change in bowel habit and malabsorption. Endoscopic and radiological features of amyloidosis are also nonspecific, with the small intestine most commonly affected. In the absence of specific treatments for GI amyloidosis, therapy is aimed at reducing or eliminating the supply of the respective fibril precursor protein. Supportive measures such as nutritional support and antidiarrheal agents should be instigated while awaiting the clinical improvement associated with a successful reduction in the abundance of the fibril precursor protein. GI tract surgery should be performed only if the benefits clearly outweigh the risks, as there is a risk of decompensation of organs affected by amyloid.

Systemic amyloidosis and the gastrointestinal tract

Systemic amyloidosis is characterized by the extracellular deposition of protein in an abnormal fibrillar form. Several different types of amyloidosis exist, each defined by the identity of their respective fibril precursor protein. Among patients with systemic amyloidosis, histological involvement of the gastrointestinal tract is very common but is often subclinical. Conversely, primary diseases of the gastrointestinal tract can cause systemic amyloidosis; for example, AA amyloidosis can occur secondary to IBD. The presence and pattern of gastrointestinal symptoms varies substantially, not only between the different types of amyloidosis but also within them. Typical clinical presentations, most of which are nonspecific, include macroglossia, hemorrhage, motility disorders, disturbance of bowel habit and malabsorption. Endoscopic and radiological features are also nonspecific, with the small intestine most commonly affected. Currently, the aim of therapy for amyloidosis is to slow amyloid formation by reducing the abundance of the fibril precursor protein. No specific treatments for the gastrointestinal symptoms of systemic amyloidosis are available; however, case reports and small published series encourage nutritional support for patients with motility disorders and pharmacological agents for treatment of diarrhea. Surgical procedures should be contemplated only in an emergency setting because of the risk of decompensation of organs affected by amyloid deposition.

Management of the Trauma Victim with Pre-Existing Endocrine Disease

The clinical course of individuals after trauma largely is determined by their pretraumatic state. The endocrine system plays a major role in the response to injury, surgery, and sepsis, and endocrine dysfunction places the trauma victim at risk of greater morbidity and mortality. Further, chronic endocrine disease usually is accompanied by multiorgan dysfunction, which may compromise the physiologic reserve of the critically injured patient. Among patients with pre-existing endocrine disease, the severe stresses of multisystem trauma can lead to a further, often subtle, decompensation in endocrine function (Fig. 1). In the management of trauma victims with pre-existing endocrine disease, the role of the critical care specialist is three-fold--(1) to maintain a high index of suspicion for endocrine disease in all trauma victims, (2) to anticipate and prevent endocrine organ decompensation, and (3) to rapidly diagnose and institute therapy in those suspected of having endocrine disease.

The natural history of hypertension

1. 1. Two hundred and twelve patients with various forms of hypertension were classified according to the changes in their optic fundi and the degree of target organ involvement. They were followed up for an average period of four years, the shortest follow-up interval being two years for any one patient. During the period of observation the patients received no antihypertensive drug therapy but were given more general medical treatment as indicated. 2. 2. Those with essential hypertension showed a strikingly different life expectancy, depending upon the presence or absence of sustained uremia. 3. 3. In the absence of sustained uremia, the degree of change in the optic fundi and the severity of other target organ involvement seemed most markedly to influence the patient's life expectancy. 4. 4. Those with elevated diastolic blood pressures, irrespective of the degree of elevation, who manifested benign changes in the optic fundi and no evidence of target organ decompensation enjoyed a life expectancy approximating that of the general population for a similar age group. 5. 5. In view of these findings and the fact that there is often marked lability in the diastolic blood pressures in patients in all stages of severity of essential hypertensive disease, evaluation of drug therapy should be based upon the degree of target organ involvement and optic fundal changes rather than upon the degree of elevation of the diastolic blood pressure.