scholarly journals A Device for Automatically Measuring and Supervising the Critical Care Patient’S Urine Output

Sensors ◽  
2010 ◽  
Vol 10 (1) ◽  
pp. 934-951 ◽  
Author(s):  
Abraham Otero ◽  
Francisco Palacios ◽  
Teodor Akinfiev ◽  
Roemi Fernández
Keyword(s):  
Critical Care ◽  
Urine Output

Measuring intraabdominal pressure

1990 ◽  
Vol 10 (3) ◽  
pp. 54-66 ◽  
Author(s):  
D Lameier ◽  
D NeCamp
Keyword(s):  
Renal Function ◽  
Critical Care ◽  
Causal Relationship ◽  
Urine Output ◽  
Clinical Parameter ◽  
Critical Care Nurses ◽  
Intraabdominal Pressure ◽  
Formal Study ◽  
Time Relationship ◽  
The Future

This article is intended to help nurses understand the physiologic rationale for the measurement of IAP. We were able to see a time relationship between increasing IAP and decreasing urine output in our patients. When measures were taken to reduce IAP, urine output improved. No causal relationship is implied because no formal study was done and many other factors may have influenced the IAP measurement and the renal function of these patients. Critical care nurses may be called upon to measure this clinical parameter more frequently in the future. Our experience with IAP may help other critical care nurses when they begin to measure the IAP of their patients.

scholarly journals An Unusual Case of Transient Diabetes Insipidus After Prolonged Vasopressin Infusion

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A572-A573
Author(s):  
Albert Chang ◽  
Dharscika Arudkumaran ◽  
Deviani Umadat ◽  
Deirdre A Cocks Eschler
Keyword(s):  
Septic Shock ◽  
Critical Care ◽  
Diabetes Insipidus ◽  
Serum Sodium ◽  
Urine Output ◽  
Care Setting ◽  
Critical Care Setting ◽  
Surgical Intensive Care Unit ◽  
Vasopressin Infusion ◽  
Neurosurgical Patients

Abstract Background: Vasopressin is a hormone produced in the hypothalamus and secreted by the posterior pituitary. Underproduction or resistance to vasopressin can lead to diabetes insipidus (DI) resulting in the imbalance of fluid status and serum sodium levels. Synthetic vasopressin is a common second line agent used in the critical care setting for its vasopressor effects with an added clinical benefit by increasing cerebral perfusion pressure. There have been reported cases of transient DI after discontinuation of vasopressin in neurosurgical patients, however only few cases have been reported in septic shock patients without neurological involvement. We present a case of transient DI during treatment for septic shock after attempts to wean off vasopressin infusion. Presentation: A 41-year-old female with history of type 2 diabetes mellitus, quadriplegia following a motor vehicle accident at age 11 was admitted to the surgical intensive care unit for urosepsis after placement of right ureteral stent. The patient was started on broad spectrum intravenous (IV) antibiotics and vasopressors norepinephrine and vasopressin. After 8 days of vasopressin treatment, with each effort to wean IV vasopressin, the patient was noted to have significant polyuria with urine output reaching as much as 800 mL/hr and increase in her serum sodium to a maximum of 148 mmol/L (n 145 mmol/L). During episodes of excessive diuresis, urine sodium reached 87 mmol/L, urine osmolality was 72 mOsm/kg (50-1400 mOsm/kg), and serum osmolality was 288 mOsm/kg (n 300 mOsm/kg). The patient received three doses of 1 microgram of desmopressin 24 hours apart while weaning off vasopressin. This helped slow excessive diuresis while also maintaining normal serum sodium levels. Urine output decreased to approximately 150 mL/hr after each administration of desmopressin. The serum sodium levels eventually stabilized between 135-140 mmol/L and urine output held steady around 200 cc/hr. The patient did not require additional desmopressin and was hemodynamically stable off all vasopressors. Discussion: The pathophysiology behind transient diabetes insipidus following vasopressin infusion is still unclear. It is known that in septic shock, there is depletion of vasopressin stores which suggests central DI. Yet, pharmacologic doses of vasopressin are speculated to downregulate V2 receptors in the renal distal convoluted tubules and collecting ducts which suggests nephrogenic DI. Our patient responded to desmopressin which indicates that she at least had a central component of DI. There is no consensus on the duration of vasopressin required to precipitate transient DI, but vasopressin infusion was administered for at least 24 hours in other cases prior to onset. We present a rare case of transient diabetes insipidus after prolonged vasopressin infusion that clinicians should be aware of in the critical care setting.

scholarly journals A Low Cost Device for Monitoring the Urine Output of Critical Care Patients

Sensors ◽  
2010 ◽  
Vol 10 (12) ◽  
pp. 10714-10732 ◽  
Author(s):  
Abraham Otero ◽  
Francisco Palacios ◽  
Teodor Akinfiev ◽  
Andrey Apalkov
Keyword(s):  
Critical Care ◽  
Urine Output ◽  
Low Cost ◽  
Critical Care Patients

Effects of cisplatin treatment on the rat neurohypophysis

1986 ◽  
Vol 44 ◽  
pp. 122-123
Author(s):  
J.M. Fadool ◽  
P.J. Boyer ◽  
S.K. Aggarwal
Keyword(s):  
Side Effects ◽  
Urine Output ◽  
Morphological Changes ◽  
Limiting Factor ◽  
Antineoplastic Drugs

Cisplatin (CDDP) is currently one of the most valuable antineoplastic drugs available. However, it has severe toxic side effects of which nephrotoxicity is the major dose limiting factor in its use. It induces morphological changes in the kidney with hampered urine output. The present study is an effort to determine the influence of the drug on the neurohypophysis for any antidiuretic effects on the kidney.

GLP-1 May Be Alternative to Insulin in Critical Care

2008 ◽  
Vol 41 (5) ◽  
pp. 30
Author(s):  
MIRIAM E. TUCKER
Keyword(s):  
Critical Care
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