Severe Hyperosmolarity Research Articles

Exploration of Baihu Jia Renshen Decoction formula syndromes based on severe cases of critical care and integrative medicine and its clinical efficacy on clearing heat,elevating blood pressure,curing hypertonic and lowering blood sugar

Baihu Jia Renshen Decoction recorded in Treatise on Febrile Diseases by Zhang Zhongjing in the Han Dynasty could be used to clear heat,invigorate Qi,and promote fluid production. The indications of Baihu Jia Renshen Decoction include infectious diseases,such as lung infection,influenza,encephalitis,enteric typhoid and hospital infection; thermoplegia; acute cerebrovascular disease,diabetes mellitus,severe hyperosmolarity,hypernatremia,intractable hypotension,shock and other internal diseases; sweating,irritation,thirst,want to drink several liters of water,dry mouth,dry tongue,and big pulse. This prescription has been widely used to treat acute and severe cases in the cardiovascular intensive care ward. The prescription can be used to treat exogenous and internal injury diseases,which are characterized by excessive heat,fluid injury,thirst for water,dry mouth,dry tongue and other symptoms; refractory hypotension and hypovolemic shock that need large dose of supplemental fluid to maintain blood pressure and may also belong to the extension of the Baihu Jia Renshen Decoction formula syndrome; severe hyperosmolarity and hypernatremia needing nasal feeding with large quantities of sterile water or cool boiled water that may also belong to the extension of the Baihu Jia Renshen Decoction formula syndrome; the four major symptoms,namely severe heat,excessive perspiration,great thirst,and large-bounding pulse,are actually the indications of Baihu Jia Renshen Decoction,rather than Baihu Decoction. Severe irritability should also be added into the indications of Baihu Jia Renshen Decoction; severe heat refers to pathogenesis,rather than a symptom.

Adipsic Diabetes Insipidus: A Single-Center Case Series

: Adipsic diabetes insipidus (ADI) is a rare and challenging complication secondary to several neurosurgical procedures. It can lead to severe hyperosmolarity and is associated with high rates of morbidity and mortality. Considering the variable time of thirst sensation recovery, long-term treatment is accompanied with the risk of extreme extracellular osmolality fluctuations. Herein, we report 3 cases of this rare presentation of hypothalamic injury.

The JNK-Like MAPK KGB-1 of Caenorhabditis Elegans Promotes Reproduction, Lifespan, and Gene Expressions for Protein Biosynthesis and Germline Homeostasis but Interferes with Hyperosmotic Stress Tolerance

Aims: This study focused on the role of the JNK-like MAPK (mitogen-activated protein kinase) KGB-1 (kinase, GLH-binding 1) for osmoprotection and other vital functions. Methods: We mapped KGB-1 expression patterns and determined lifespan, reproduction and survival rates as well as changes in body volume, motility, and GPDH (glycerol-3-phosphate dehydrogenase) activity for glycerol production in wildtype (WT), different signaling mutants (including a kgb-1 deletion mutant, kgb-1∆) and RNAi-treated worms under control and hyperosmotic conditions. KGB-1-mediated gene expressions were studied, for instance, by RNA Sequencing, with the resulting transcriptome data analyzed using orthology-based approaches. Results: Surprisingly, mutation/RNAi of kgb-1 and fos-1 (gene for an AP-1, activator protein 1, element) significantly promoted hyperosmotic resistance, even though hyperosmotic GPDH activity was higher in WT than in kgb-1∆. KGB-1 and moderate hyperosmolarity promoted and severe hyperosmolarity repressed kgb-1, fos-1, and jun-1 (gene for another AP-1 element) expression. Transcriptome profiling revealed, for instance, down-regulated genes for protein biosynthesis and up-regulated genes for membrane transporters in kgb-1∆ and up-regulated genes for GPDH-1 or detoxification in WT, with the latter indicating cellular damage and less effective osmoprotection in WT. Conclusion: KGB-1 promotes reproduction and lifespan and fosters gene expressions for AP-1 elements, protein biosynthesis, and balanced gametogenesis, but inhibits expressions for membrane transporters perhaps in order to control energy consumption. Reduced protein biosyntheses and enhanced membrane transports in kgb-1∆ most likely contribute to the high hyperosmotic tolerance of the mutant by easing the burden of the existing chaperone machinery and promoting regulatory volume increases upon hyperosmotic stress.

Severe hyperosmolarity and hypernatremia in an adipsic young woman

Combined deficits in arginine vasopressin secretion (AVP) and thirst sensation can result in life threatening hyperosmolality and hypernatremia. Complications include seizures, profound volume contraction and renal failure. Fortunately, this is an uncommon clinical condition, with approximately 70 cases reported in the literature over the past 47 years [1]. Defects in AVP secretion and/or synthesis produce central diabetes insipidus (DI), polyuria with polydipsia, hypernatremia and hyperosmolality. Most awake and alert patients with an intact thirst stimulus will "drink" themselves back to a normal serum sodium and osmolality. However, if there is concomitant destruction of the osmoreceptors that regulate thirst, osmolal and volume homeostasis cannot be maintained. The relationships between urine osmolarity and serum osmolarity and plasma vasopressin levels are vital for distinguishing a reset osmostat from central DI. After obtaining approval from our institutional review board, we retrospectively reviewed the medical record of a 37-year-old patient who presented to our institution with a serum sodium of 176 mEq/l. Admission laboratory examination revealed: hemoglobin 12.8 g/dl; white blood cell count 4.7 × 103/µl, with a normal differential; random serum glucose 91 mg/dl ; sodium 176 mEq/l; plasma osmolality 366 mOsm/kg; BUN 33 mg/dl; serum creatinine 1 mg/dl; calcium 9.5 mg/dl; urine specific gravity 1.032; and urine osmolality 1,172 mOsm/kg. An MRI with contrast of the sella/ pituitary revealed an enhancing mass centered within the suprasellar cistern and anterior third ventricle, measuring 3.0 × 3.9 × 3.4 cm. The lesion appeared to involve the hypothalamus and displaced the optic chiasm inferiorly. Evaluation of pituitary function revealed normal serum levels of thyroid stimulating hormone, AM cortisol, luteinizing hormone, follicle stimulating hormone and prolactin. Figure 1 illustrates the relationship between measured serum AVP levels and serum osmolality. Figure 2 shows the relationship between measured urine and serum osmolality. If the serum AVP levels were not available, it would appear as though the patient had a reset osmostat. The kidneys appear to appropriately generate maximally concentrated urine at a serum osmolality above 348 but are unable to below this value. When compared with the normal curve, our patient's AVP levels were lower than expected for the corresponding osmolality. This pattern is consistent with a partial central DI. She does not have a reset osmostat. In the presence of significant volume contraction and a reduced GFR, her kidneys produced more concentrated urine despite markedly decreased central vasopressin production. As the volume contraction abated and the GFR improved, polyuria recurred, despite persistent hyperosmolarity and hypernatremia.

Acute hyperglycemic emergencies in children with type 2 diabetes

Acute hyperglycemic emergencies in children with type 2 diabetes

Acute myocardial infarction in a 12-year-old as a complication of hyperosmolar diabetic ketoacidosis.

OBJECTIVE: This report describes the evolution of an acute myocardial infarction in a 12-yr-old male with severe hyperosmolarity secondary to diabetic ketoacidosis. DESIGN: Case report. SETTING: Intensive care unit of a university teaching hospital. Patient: A 12-yr-old male with new-onset diabetic ketoacidosis and an abnormal electrocardiogram. MEASUREMENTS AND MAIN RESULTS: The evolution of an acute myocardial infarction in this patient is described. This includes serial electrocardiographic, echocardiographic, and enzymatic changes. Early recognition of this complication of diabetic ketoacidosis prompted immediate initiation of antithrombotic therapy and possible prevention of infarct extension. CONCLUSION: This report demonstrates the need for accurate electrocardiographic monitoring in these patients, both for arrhythmias as well as ischemic changes and the potential for myocardial injury caused by hyperosmolarity.