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Urine output
Published in Hemanshu Prabhakar, Charu Mahajan, Indu Kapoor, Manual of Neuroanesthesia, 2017
Central neurogenic diabetes insipidus is often associated with TBI, neurosurgeries, tumor, increased intracranial pressure, brain death, and central nervous system infections. Development of diabetes insipidus (DI) in nonpituitary surgery is associated with severe, preterminal cerebral edema. It is a common finding after brainstem death and also an important feature for management in organ donors.6
Chronic Posttraumatic Stress
Published in Rolland S. Parker, Concussive Brain Trauma, 2016
Impact can lead to transection of the pituitary stalk. Lesions of the hypothalamic supraoptic nuclei, the infundibulum, and the upper half of the pituitary stalk can denervate the posterior lobe of the pituitary (Crompton, 1971). After head trauma, there is sudden appearance of hypotonic polyuria consequent to interference with the transport of vasopressin (a water retaining, or ADH), which is synthesized in the paraventricular and supraoptic nuclei of the hypothalamus, and is transported down the long axons that comprise the supraopticohypophyseal tract to terminate in the posterior pituitary (Robinson, 1996). It is observed in children and adults, may occur within 24 h after injury, and resolves in only half of cases; the remaining half suffer from permanent vasopressin deficiency (Bode et al., 1996; Findling & Tyrell, 1986). Interruption of the blood supply to the hypothalamus and pituitary leads to neurogenic diabetes insipidus (Ramsey, 1986). Accidental head injuries may result in diabetes insipidus within 24 h after injury (Bode et al., 1996). In about half of these patients the disease resolves spontaneously. Some children recovering from traumatic stalk section and transient diabetes insipidus form an ectopic posterior pituitary.
Endocrine diseases and pregnancy
Published in Hung N. Winn, Frank A. Chervenak, Roberto Romero, Clinical Maternal-Fetal Medicine Online, 2021
Diabetes insipidus (DI) is the inability to concentrate urine, owing to AVP deficiency [central or neurogenic diabetes insipidus (CDI)] or renal tubular resistance to AVP (nephrogenic diabetes insipidus) (55). Causes of CDI include head trauma and hypothalamic tumors and other anatomic lesions; many cases are idiopathic. Transient forms of CDI may occur in pregnancy, owing to unmasking of subclinical disease by circulating vasopressinase (56) or to excessive circulating vasopressinase in the setting of hepatic dysfunction (57). Other causes of polyuria should be excluded by appropriate and pragmatic patient assessment. Diabetes mellitus causes polyuria, but if so, it is always accompanied by glycosuria. Urine dipstick consistently negative for glucose excludes this possibility. So long as thirst sensation is intact, plasma osmolality remains normal if patients are able to drink and have access to water. In the presence of CDI or nephrogenic DI, nonavailability of water or inability of the patient to drink because of nausea, vomiting, or impaired cognition will quickly result in dehydration and hyperosmolar hypernatremia. Various forms of dipsogenic DI also occur, but since AVP secretion and response are typically normal, a strong clinical clue suggestive of dipsogenic DI is significant hypoosmolar hyponatremia (as opposed to slight hypernatremia or normal serum sodium concentration, which is expected in either CDI or nephrogenic DI). Dipsogenic DI is commonly due to a primary psychiatric disorder—notably, schizophrenia—or may be due to hypothalamic disorders (e.g., neurosarcoidosis), which reset the “osmostat” for thirst.
Clinical, laboratory and genetic features of Erdheim-Chester disease patients: analysis of a retrospective cohort of two reference centers in Latin America
Published in Hematology, 2022
Antonio Adolfo Guerra Soares Brandão, André Ramires Neder Abdo, Luís Alberto de Pádua Covas Lage, Giancarlo Fatobene, Juliana Pereira, Vanderson Rocha
In our cohort, the main ECD involved organ was bone (75% – 12/16), followed by skin (43.8% – 7/16), central nervous system (CNS) (43.8% – 7/16), lymph node (25% – 4/16), lung (12.5% – 2/16), liver (6.3% – 1/16), spleen (6.3% – 1/16), muscle (6.3% – 1/16) and gastrointestinal tract (6.3% – 1/16). The majority of CNS lesions occurred in the pituitary gland (86% – 6/7). Twelve patients (75%) presented involvement of more than one organ, characterizing a multi-organic form. Xanthelasma and xanthomas were the most common skin lesions. The most frequent clinical manifestations were bone pain (43.8% – 7/16) and neurogenic diabetes insipidus (37.5% – 6/16). Osteosclerotic lesions occurred in 75% (12/16) of cases, retroperitoneal fibrosis and thickening of the renal fascia (‘hairy kidney’ or ‘perinephric straining’) in 37.5% (6/16), 25% (4/16) presented coated aortic sign, and orbital infiltration was found in 25% (4/16), constituting the highly specific features for the diagnosis of ECD. Table 1 summarizes the main clinical-molecular characteristics, therapeutic modalities and responses of the 16 Brazilian patients with ECD included in our analysis.
Hypotension on admission in patients with isolated traumatic brain injury: contemporary examination of the incidence and outcomes using a national registry
Published in Brain Injury, 2020
Alexander Becker, Yehuda Hershkovitz, Kobi Peleg, Joseph Dubose, Givon Adi, Zahalka Aala, Boris Kessel
The mechanism of hypotension in patients with traumatic brain injuries is not well defined. Pop et al. studied hemodynamics in patients with severe brain injuries, finding that the cardiac index on admission in all patients was low (20). Cardiovascular response to severe brain injury likely consists of decreased cardiac contractility and stroke volume, arrhythmias, decreased peripheral vascular resistance, and heart failure through complex mechanisms (21). Other potential causes to hypotension among patients with TBI include iatrogenic sequela, such as the use of midazolam or etomidate for intubation (22). In addition, intravascular volume depletion may result in this unique population due to polyuria secondary to acute onset of neurogenic diabetes insipidus (23).