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A pensioner with ‘waterworks’ problems
Published in Tim French, Terry Wardle, The Problem-Based Learning Workbook, 2022
In mild diuresis, increased oral fluid intake should suffice; however some patients may lose large volumes of urine, becoming significantly dehydrated. This may be so severe as to cause postural hypotension or collapse. Close monitoring of urine output is necessary. If patients pass more than 200 ml of urine for a prolonged period of time (>5 hours) then i.v. replacement is necessary. Care should be taken not to ‘over-replace’ fluid losses since this will just lead to further diuresis. A practical fluid replacement regime is to replace half of the preceding hour’s urine output with intravenous saline.
Emergency Surgery
Published in Tjun Tang, Elizabeth O'Riordan, Stewart Walsh, Cracking the Intercollegiate General Surgery FRCS Viva, 2020
Alastair Brookes, Yiu-Che Chan, Rebecca Fish, Fung Joon Foo, Aisling Hogan, Thomas Konig, Aoife Lowery, Chelliah R Selvasekar, Choon Sheong Seow, Vishal G Shelat, Paul Sutton, Colin Walsh, John Wang, Ting Hway Wong
What is the pathophysiology of post-obstructive diuresis?From a physiological perspective, post-obstructive diuresis occurs due to an accumulation of electrolytes, fluid and waste products. When the obstruction is relieved, these substances are then released. Pathological diuresis occurs due to dysfunction of renal tubules and inappropriate salt and water handling by the kidney.
The endocrine system
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
The loss of glucose via the urine promotes an osmotic diuresis, causing dehydration and thirst. In the liver, excess free fatty acids are converted into ketone bodies, which, in the absence of available glucose, are metabolized for cellular energy. The ketone bodies produce a metabolic acidosis (ketoacidosis). If untreated this metabolic disturbances produces hyperosmolarity, hypovolaemia, acidosis, and electrolyte imbalance, which have serious effects on the functions of neurons and result in diabetic ketoacidosis.
Comparison between different anaesthesia techniques for protecting renal function in children undergoing radical nephrectomy
Published in Egyptian Journal of Anaesthesia, 2022
Hassan Saeed ELHoshy, Islam Mohamed ELBardan
The underlying mechanism by which Dex. exerts its reno-protective effect is multifactorial [27,28]. Several advances revealed stimulation of alpha-2 agonists, inhibits surgical neuro-hormonal stress response with subsequent decrease of catecholamine release, thus providing hemodynamic stability and optimum renal condition. Also, nitric oxide mediated vasodilation process occurs due to selective α-2 adrenoceptor, which are numerous in the renal peritubular structure with resultant increase in renal blood flow and glomerular filtration rate. Moreover, diuresis occurs via inhibition of renin and arginine- vasopressin system leading to decrease of sodium and water reabsorption. Additionally, current evidence demonstrated the role of Dex. in kidney protection from reactive oxygen peroxides generated during ischemia -reperfusion phases in radical nephrectomy [27–29].
Impact of chronic medications in the perioperative period: mechanisms of action and adverse drug effects (Part I)
Published in Postgraduate Medicine, 2021
Ofelia Loani Elvir-Lazo, Paul F White, Hillenn Cruz Eng, Firuz Yumul, Raissa Chua, Roya Yumul
Common adverse effects associated with diuretics include electrolyte imbalances, acid/base disturbances, and dehydration secondary to excessive diuresis [25]. Thiazide and loop diuretics inhibit sodium reabsorption proximal to the collecting tubule at the aldosterone-mediated Na/K pump, which results in compensatory potassium efflux in an effort to reabsorb sodium producing hyponatremia and hypokalemia [25]. Potassium-sparing diuretics, on the other hand inhibit the Na/K pump at the collecting duct minimizing the risk of hypokalemia [24]. Thiazide and loop diuretics can potentially cause metabolic alkalosis, whereas potassium-sparing diuretics may cause metabolic acidosis. Other potential adverse effects of thiazides include sulfonamide allergies, hyperglycemia, and hyperuricemia (gout). [25]
Rapidly progressive fatal hypoxia in a young woman
Published in Baylor University Medical Center Proceedings, 2021
Aaron J. Sohn, Joseph M. Guileyardo, Alastair J. Moore, Kenneth A. Ausloos, Chetan A. Naik
The patient was initiated on upfront dual therapy for pulmonary arterial hypertension with tadalafil 20 mg once daily and ambrisentan 5 mg once daily. The following day, her oxygen requirements increased from 3 L/min to 6 L/min, and chest x-ray revealed new pulmonary edema, raising a concern for pulmonary veno-occlusive disease (PVOD). Tadalafil and ambrisentan were discontinued and intravenous furosemide was initiated, resulting in improvement in oxygen requirement back to 3 L/min over the next 3 days. Inpatient evaluation for lung transplantation could not be pursued due to lack of medical insurance. However, with aggressive diuresis, the patient developed progressive hypotension and acute kidney injury over the next 2 weeks and sustained cardiac arrest with pulseless electrical activity. She died despite attempted resuscitation, and the family consented to autopsy.