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. 2017 Nov;107:429-436.
doi: 10.1016/j.wneu.2017.07.175. Epub 2017 Aug 7.

Physiologic Mechanisms of Water and Electrolyte Disturbances After Transsphenoidal Pituitary Surgery

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Free PMC article

Physiologic Mechanisms of Water and Electrolyte Disturbances After Transsphenoidal Pituitary Surgery

Evan T Blair et al. World Neurosurg. .
Free PMC article

Abstract

Background: Disturbances in water and electrolyte homeostasis are common after transsphenoidal surgery. These disorders are variable and unpredictable, increasing patient risk and complicating postsurgical treatment. Clinically, it is generally accepted that damage to the pituitary is the cause, but the mechanisms behind the response variability and underlying pathophysiology remain unknown.

Objective: To test the hypothesis that changing the degree of damage to the pituitary stalk produces a spectrum of water and electrolyte disturbance along which all presentations of postsurgical water and electrolyte disturbances can be identified.

Methods: We used HumMod, a large mathematical model of physiology, to simulate pituitary stalk damage at differing fractions: 20%, 40%, 60%, and 80%. The damaged neurons were modeled to undergo a 5-day countdown to degeneration and release stored antidiuretic hormone as they die, as is proposed to occur.

Results: Lower pituitary damage (20%) resulted in transient polyuria and intermediate damage (40%) was associated with delayed polyuria and diabetes insipidus. Higher levels of damage (60% and 80%) showed a triphasic pattern of diabetes insipidus.

Conclusions: We postulate that our model provides a plausible mechanistic explanation for some varieties of postsurgical water and electrolyte disturbances, in which increasing damage to the pituitary potentiates the likelihood of a full triphasic response. However, our simulation shows that merely modifying the level of damage does not produce every presentation of water and electrolyte imbalance. This theory suggests that other mechanisms, which are still unclear and not a part of this model, may be responsible for postoperative hyponatremia and require further investigation.

Keywords: Antidiuretic hormone; Mathematical modeling; Transsphenoidal pituitary surgery.

Conflict of interest statement

Conflict of interest statement: This work is supported by the Hearin Foundation through the Medical Student Research Program (MSRP), T32 HL105324 and HL 51971 grants.

Figures

Figure 1
Figure 1
Profiles of urine volume (A) and water intake (B) in response to varying degrees of pituitary damage. 20% pituitary damage produces transient polyuria, 40% a delayed polyuria with a degree of permanent diabetes insipidus, and 60 and 80% a triphasic diabetes insipidus. The corresponding plasma antidiuretic hormone (ADH) concentrations are shown full-scale (C) and with a magnified scale (D) to show fine changes
Figure 2
Figure 2
Plasma osmolarity (A) and sodium (B) levels increased during periods of polyuria and polydipsia, although these values never reached abnormally high values. Urine osmolarity (C) decreased during periods of low antidiuretic hormone levels, and vice versa.
Figure 3
Figure 3
During periods of overt polyuria (>40% pituitary damage), there were decreases in plasma volume (A) and extracellular fluid volume (B), but this was accompanied by a compensatory increase in fluid intake. Total extracellular sodium mass (C) mirrored plasma volume.
Figure 4
Figure 4
Mean arterial pressure (A), cardiac output (B), and total peripheral resistance (C) changed in accordance with fluctuating volume status but returned toward baseline values.
Figure 5
Figure 5
Decreases in glomerular filtration rate (A) were seen in the simulations that involved the lower antidiuretic hormone levels of diabetes insipidus. Aside from minor fluctuations on day 1, renal blood flow (B) and sodium excretion (C) remained relatively stable.
Figure 6
Figure 6
Tubular water reabsorption in the proximal tubule (PT) (A), Loop of Henle (B), distal tubule (DT) (C), and collecting duct (CD) (D). The most pronounced difference between the presence and absence of antidiuretic hormone was seen in the distal tubule (C) and collecting duct (D).
Figure 7
Figure 7
Atrial natriuretic peptide (ANP) increased in response to antidiuresis and decreasing in association with diabetes insipidus–induced polyuria (A). The most consistent change in the renin-angiotensin system was the decrease in angiotensin II (B) and aldosterone (C) on day 1 after the surgery.

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