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Thrombosis Research Mar 2017Ovarian hyperstimulation syndrome (OHSS) is a serious iatrogenic complication of ovarian stimulation. It is feasible to identify patients at risk, modify stimulation... (Review)
Review
Ovarian hyperstimulation syndrome (OHSS) is a serious iatrogenic complication of ovarian stimulation. It is feasible to identify patients at risk, modify stimulation strategies to ameliorate risk, and initiate out-patient treatments that alter disease pathophysiology to reduce disease severity. Mitigation of OHSS risk and severity, through innovative approaches prior to treatment, during treatment and after treatment should now be standard care. This review summarizes recent developments and provides recommendations on the prevention and treatment of OHSS.
Topics: Aspirin; Calcium Gluconate; Cyclooxygenase Inhibitors; Disease Management; Dopamine Agonists; Female; Gonadotropin-Releasing Hormone; Humans; Hypoglycemic Agents; Metformin; Ovarian Hyperstimulation Syndrome; Ovulation Induction
PubMed: 28262238
DOI: 10.1016/S0049-3848(17)30070-1 -
Cureus Jan 2022Hypocalcemia can manifest as a variety of presentations, ranging from neuromuscular irritability to seizures, and psychiatric manifestations such as emotional...
Hypocalcemia can manifest as a variety of presentations, ranging from neuromuscular irritability to seizures, and psychiatric manifestations such as emotional instability, anxiety, and depression. Here, we present a unique case of hypocalcemia-induced acute psychosis. A 24-year-old woman presented to the emergency department (ED) with confusion and agitation for four to five days. The patient was noted by the family to have decreased oral intake and sleep. Auditory and visual hallucinations prompted the family to bring the patient to the ED. The patient was mildly tachycardic. Initially, the patient was agitated, impulsive, and aggressive, exhibiting psychotic features including visual hallucinations, paranoid delusions, thought broadcasting, tangential and perseverative thought processes, and erotomanic delusions. She had mild leukocytosis and elevated procalcitonin on admission. A thorough workup ruled out infectious/inflammatory processes. Cerebrospinal fluid was negative for acute meningitis/encephalitis, autoimmune encephalitis antibodies, and paraneoplastic etiology. Thyroid-stimulating hormone was normal and thyroid antibodies were negative. The CT brain and MRI brain were unremarkable. The patient was severely hypocalcemic (6.7) with low parathyroid hormone (<6) on admission. To note, the patient has multiple endocrine neoplasia, type 2B (MEN2B). She underwent total thyroidectomy five months prior for metastatic medullary thyroid carcinoma complicated by postsurgical hypoparathyroidism. The patient had been non-compliant with calcium and calcitriol supplementation postoperatively. The patient was started on IV calcium gluconate and transitioned to calcitriol with calcium level improvement over the next three days. She experienced marked improvement, with the resolution of her psychosis. The patient's subacute onset psychosis with no personal or family psychiatric history and a rapid response to calcium correction supports hypocalcemia etiology. This case illustrates new-onset acute psychosis in a patient with calcium regulation imbalance. The development of hypocalcemia secondary to thyroidectomy with postsurgical hypoparathyroidism and calcium supplement non-compliance precipitated psychosis. A few similar cases have been reported, and here, we note that treatment of hypocalcemia promptly resolves symptoms. As per our review, this will be the first case of neuropsychiatric symptoms without associated cortical calcifications seen on imaging. It is important to recognize hypocalcemia as a rare cause of psychosis so as to not mistakenly categorize such presentations as primary psychotic disorders and miss a medically treatable illness.
PubMed: 35145781
DOI: 10.7759/cureus.20874 -
BMJ Case Reports Feb 2020A 62-year-old woman with chronic kidney disease stage 4, sleep apnoea on continuous positive airway pressure and recent admission for acute-on-chronic diastolic heart...
A 62-year-old woman with chronic kidney disease stage 4, sleep apnoea on continuous positive airway pressure and recent admission for acute-on-chronic diastolic heart failure presented to emergency room with weakness. She was hypotensive and had symptomatic bradycardia in the 30 s secondary to hyperkalaemia and beta-blockers, raising concern for BRASH syndrome. Antihypertensives were immediately held. Potassium-lowering agents (with calcium gluconate for cardiac stability) were begun, as were fluids and dopamine for vasopressor support. The patient was admitted to intensive care unit and electrophysiology was consulted. Over the next 2 days, the patient clinically improved: she remained off dopamine for over 24 hours; potassium levels and renal function improved; and heart rate stabilised in 60 s. The patient was eventually discharged and advised to avoid metolazone, bumetanide and carvedilol, with primary care provider and cardiology follow-up.
Topics: Antihypertensive Agents; Atrioventricular Block; Bradycardia; Bumetanide; Carvedilol; Female; Humans; Hyperkalemia; Metolazone; Middle Aged; Renal Insufficiency; Shock; Syndrome; Vasoconstrictor Agents
PubMed: 32094236
DOI: 10.1136/bcr-2019-233825 -
BMJ Case Reports 2009A 22-year-old Chinese man presented with sudden onset of generalised muscular weakness and paralysis upon awakening in the morning, due to sporadic periodic paralysis...
A 22-year-old Chinese man presented with sudden onset of generalised muscular weakness and paralysis upon awakening in the morning, due to sporadic periodic paralysis (SPP), a type of hypokalaemic periodic paralysis (HPP) without hyperthyroidism or familial history of paralysis. Laboratory studies showed marked hypokalaemia (K(+) 1.6 mmol/litre). He received intravenous KCl supplementation at a rate of 0.14 mmol/kg/h and developed a paradoxical fall in serum K(+) concentration from 1.6 to 1.4 mmol/litre during KCl therapy. After 160 mmol KCl supplementation his muscular strength recovered, but muscular paralysis recurred 2 h later. Acute recurrent hypokalaemia was the presumptive initial diagnosis and intravenous KCl supplementation was briefly reinitiated. Despite no obvious abnormalities on ECG monitoring, a 12-lead ECG clearly demonstrated tented T waves in the precordial leads suggestive of hyperkalaemia, later found to be 6.9 mmol/litre. After treatment with intravenous calcium gluconate, insulin and loop diuretics, his serum K(+) concentration fell to 4.7 mmol/litre and muscular paralysis resolved in 3 h.
PubMed: 21686739
DOI: 10.1136/bcr.07.2008.0577 -
Turkish Journal of Emergency Medicine 2022Intravenous (IV) calcium salts are routinely recommended as a cardio-protective therapy in the emergency treatment of severe hyperkalemia. However, this recommendation...
OBJECTIVES
Intravenous (IV) calcium salts are routinely recommended as a cardio-protective therapy in the emergency treatment of severe hyperkalemia. However, this recommendation is supported by a low level of evidence and is anecdotal. The aim of this study is to determine the effectiveness of IV Calcium (Ca) gluconate in the treatment of hyperkalemia.
MATERIALS AND METHODS
Patients with hyperkalemia and with the electrocardiogram (ECG) changes due to hyperkalemia over a 1 year period were included in this prospective observational study. Patients' ECGs were measured, before and after IV Ca-gluconate treatment and after normalization of potassium levels. Wilcoxon test and McNemar's test were used to compare the ECG parameters before and after Ca-gluconate therapy.
RESULTS
The mean potassium value of 111 patients who met the inclusion criteria was 7.1 ± 0.6 mmol/l. In this study, a total of 243 ECG pathology related to hyperkalemia, 79 of which included main rhythm disorders, and the remaining 164 were nonrhythm disorders in ECG parameters, were analyzed. No statistically significant changes were determined in patients' nonrhythm ECG disorders with IV Ca-gluconate treatment ( = 0.125). However, nine of the 79 main rhythm disorders due to hyperkalemia improved with calcium gluconate treatment and this change was statistically significant ( < 0.004).
CONCLUSION
IV Ca-gluconate therapy was found to be effective, albeit to a limited degree, in main rhythm ECG disorders due to hyperkalemia, but it was not found to be effective in nonrhythm ECG disorders due to hyperkalemia. Therefore, Ca-gluconate may be effective only in the main rhythm disorders due to hyperkalemia.
PubMed: 35529029
DOI: 10.4103/2452-2473.342812 -
Frontiers in Veterinary Science 2020Cardiopulmonary arrest (CPA), the acute cessation of blood flow and ventilation, is fatal if left untreated. Cardiopulmonary resuscitation (CPR) is targeted at restoring... (Review)
Review
Cardiopulmonary arrest (CPA), the acute cessation of blood flow and ventilation, is fatal if left untreated. Cardiopulmonary resuscitation (CPR) is targeted at restoring oxygen delivery to tissues to mitigate ischemic injury and to provide energy substrate to the tissues in order to achieve return of spontaneous circulation (ROSC). In addition to basic life support (BLS), targeted at replacing the mechanical aspects of circulation and ventilation, adjunctive advanced life support (ALS) interventions, such as intravenous fluid therapy, can improve the likelihood of ROSC depending on the specific characteristics of the patient. In hypovolemic patients with CPA, intravenous fluid boluses to improve preload and cardiac output are likely beneficial, and the use of hypertonic saline may confer additional neuroprotective effects. However, in euvolemic patients, isotonic or hypertonic crystalloid boluses may be detrimental due to decreased tissue blood flow caused by compromised tissue perfusion pressures. Synthetic colloids have not been shown to be beneficial in patients in CPA, and given their documented potential for harm, they are not recommended. Patients with documented electrolyte abnormalities such as hypokalemia or hyperkalemia benefit from therapy targeted at those disturbances, and patients with CPA induced by lipid soluble toxins may benefit from intravenous lipid emulsion therapy. Patients with prolonged CPA that have developed significant acidemia may benefit from intravenous buffer therapy, but patients with acute CPA may be harmed by buffers. In general, ALS fluid therapies should be used only if specific indications are present in the individual patient.
PubMed: 33585610
DOI: 10.3389/fvets.2020.625361 -
Cureus Jan 2024Hyperkalemia has been defined as a condition where a serum potassium level is >5.5 mmol/l. It is associated with fatal dysrhythmias and muscular dysfunction. Certain... (Review)
Review
Hyperkalemia has been defined as a condition where a serum potassium level is >5.5 mmol/l. It is associated with fatal dysrhythmias and muscular dysfunction. Certain medical conditions, such as chronic kidney disease (CKD), diabetes mellitus, and others, can lead to hyperkalemia. Many of the signs of hyperkalemia are nonspecific. A history and physical examination can be beneficial in the diagnosis of the condition. In this regard, certain characteristic electrocardiogram findings are associated with hyperkalemia along with laboratory potassium levels. In acute and potentially lethal conditions, hyperkalemia treatments include glucose and insulin, bicarbonate, calcium gluconate, beta-2 agonists, hyperventilation, and dialysis. There are several drugs, both old and new, that can additionally aid in the reduction of serum potassium levels. The present investigation evaluated some of these different drugs, including sodium polystyrene sulfonate (SPS), sodium zirconium cyclosilicate (SZC), and patiromer. These drugs each have increased selectivity for potassium and work primarily in the gastrointestinal (GI) tract. Each of these medications has unique benefits and contraindications. Clinicians must be aware of these medications when managing patients with hyperkalemia.
PubMed: 38406030
DOI: 10.7759/cureus.52994 -
Bioactive Materials Oct 2023The management of diabetic wounds remains a critical therapeutic challenge. Platelet-rich plasma (PRP) gel, PRP-derived exosomes (PRP-Exos), and mesenchymal stem...
Engineering homologous platelet-rich plasma, platelet-rich plasma-derived exosomes, and mesenchymal stem cell-derived exosomes-based dual-crosslinked hydrogels as bioactive diabetic wound dressings.
The management of diabetic wounds remains a critical therapeutic challenge. Platelet-rich plasma (PRP) gel, PRP-derived exosomes (PRP-Exos), and mesenchymal stem cell-derived exosomes (MSC-Exos) have demonstrated therapeutic potential in wound treatment. Unfortunately, their poor mechanical properties, the short half-lives of growth factors (GFs), and the burst release of GFs and exosomes have limited their clinical applications. Furthermore, proteases in diabetic wounds degrade GFs, which hampers wound repair. Silk fibroin is an enzyme-immobilization biomaterial that could protect GFs from proteases. Herein, we developed novel dual-crosslinked hydrogels based on silk protein (SP) (sericin and fibroin), including SP@PRP, SP@MSC-Exos, and SP@PRP-Exos, to promote diabetic wound healing synergistically. SP@PRP was prepared from PRP and SP using calcium gluconate/thrombin as agonist, while SP@PRP-Exos and SP@MSC-Exos were derived from exosomes and SP with genipin as crosslinker. SP provided improved mechanical properties and enabled the sustained release of GFs and exosomes, thereby overcoming the limitations of PRP and exosomes in wound healing. The dual-crosslinked hydrogels displayed shear-induced thinning, self-healing, and eradication of microbial biofilms in a bone-mimicking environment. , the dual-crosslinked hydrogels contributed to faster diabetic wound healing than PRP and SP by upregulating GFs expression, down-regulating matrix metalloproteinase-9 expression, and by promoting an anti-NETotic effect, angiogenesis, and re-epithelialization. Hence, these dual-crosslinked hydrogels have the potential to be translated into a new generation of diabetic wound dressings.
PubMed: 37234363
DOI: 10.1016/j.bioactmat.2023.05.002