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Revista Española de Cirugía Oral y Maxilofacial

On-line version ISSN 2173-9161Print version ISSN 1130-0558

Rev Esp Cirug Oral y Maxilofac vol.27 n.1 Madrid Jan./Feb. 2005


Artículo Clínico

Hydroelectrolytic disorders following orthognathic surgery

Trastornos hidroelectrolíticos en el postoperatorio de cirugía ortognática


L. García-Arana1, J.L. Cebrián2, R. Uña3, M.J. Morán2, E. Gómez García2, V. Martorell4

Abstract: Introduction. The aim of this article is to analize the early polyuria cases that we found among our patients that have undergone a orthognatic procedure.
Materials and methods. We reviewed data from 172 patients that have undergone an orthognatic surgycal procedures between 1997 and 2002. We collected data during the intraoperatory period, and the first 24 postoperatory hours.
Results. 55% of the patients that staid for more than 24 hours in Reanimation showed early autolimited polyuria. All of them were successfully treated with a proper hidroelectrolitic treatment. One needed intranasal desmopresin. However hypopotasemy in one case and hyponatremy in another were resolved with hidroelectrolitic treatment.
Disscusion and conclusions. Almost 50% of patients surgically treated of dentofacial deformities present polyuria in the early postoperatory period. There are three main etiologic hypotesis: hydric intoxication during surgery, inhibition of ADH liberation due to facial osteotomies, and salt wasting syndrome. The most probable in our serie is an hydric intoxication during surgery.

Key words: Orthognatic surgery; ADH; SALT wasting síndrome; Hydroelectrolitic balance.

Resumen: Objetivo. El objetivo de este trabajo es analizar los cuadros de poliuria precoz encontrados en un alto porcentaje de nuestros pacientes sometidos a procedimientos de cirugía ortognática.
Material y método.
Hemos realizado un estudio descriptivo retrospectivo, a partir de la revisión de las historias clínicas de los 172 pacientes sometidos a cirugía ortognática entre los años 1997 y 2002, con el fin de recoger datos analíticos y de diuresis referentes tanto a la cirugía como al período de estancia en Reanimación.
Un 55% de los pacientes que ingresaron en la unidad de reanimación postoperatoria presentaron poliurias precoces autolimitadas. Todas fueron tratadas con éxito con un correcto manejo hidroelectrolítico, salvo un caso que necesitó desmopresina intranasal. Dos pacientes presentaron alteraciones iónicas: un caso de hipopotasemia y otro de hiponatremia. Ambos respondieron adecuadamente a la reposición hidroelectrolítica.
Discusión y conclusiones.
Casi el 50% de los pacientes tratados de deformidades dentofaciales mediante cirugía ortognática desarrolla poliuria en el postoperatorio inmediato. Las tres hipótesis etiológicas que barajamos fueron: una intoxicación hídrica producida en el quirófano, una inhibición de la producción hipofisaria de hormona antidiurética tras las osteotomías faciales y un síndrome de gasto de sal relacionado con excreción inadecuada del péptido atrial natriurético. En nuestros casos lo más probable es que se trate de una intoxicación hídrica producida durante la cirugía, que haga replantearse el manejo de líquidos en el período perioperatorio.

Palabras clave: Cirugía ortognática; ADH; Síndrome pierde sal; Equilibrio hidroelectrolítico.

Recibido: 11-03-2004

Aceptado: 16-04-2004

1 Médico residente de Cirugía Oral y Maxilofacial
2 Médico adjunto de Cirugía Oral y Maxilofacial
3 Médico adjunto de Anestesiología y Reanimación
4 Jefe de Servicio de Cirugía Oral y Maxilofacial
Hospital Universitario La Paz. Madrid, España.

Dra. Laura García Arana
C/Antonio López Aguado 4, 10º A izq
28029-Madrid, España.



When managing postoperative patients, adequate control of their hydroelectrolytic balance is fundamental.

Alterations in osmoregulation observed after craniofacial surgery (equally in patients with congenital deformities as in oncological patients) or following craniofacial trauma, are common and well-known complications. They become clinically manifest as early polyuria.1-3 Similar symptoms have also been described following spinal cord surgery or traumatism. 4,5

If diagnosed rapidly these are easy to control with adequate treatment but, if overlooked, they can lead to a cerebral edema, increased intracranial pressure and death due to circulatory compromise.1

The etiology of this clinical situation is not completely known. When the first cases were described at the end of the 70s and at the beginning of the 80s, they were attributed to symptoms of central diabetes insipidus, during which there would be a transitory inhibition of the neurohypophysis resulting in a reduction of ADH secretion.6 During the last few years other theses have been but forward such as salt wasting and losses related to an inadequate secretion of peptide or atrial natriuretic factor.1,2

References in the international literature to these syndromes in patients suffering from pathological changes exclusively in the maxillofacial area are scarce and practically anecdotal,7,8 as most publications present cases of craniofacial surgery with intracranial approaches (fundamentally in the sellar region).3,6,9

However, in our experience of patients with dentofacial deformities requiring corrective orthognathic surgery, we have observed how with a certain frequency symptoms of polyuria with hyponatremia appear during the first few days of the postoperative period.

In order to evaluate the characteristics of these clinical symptoms, we have carried out a retrospective study that includes all the patients operated for orthognathic surgery by the Service of Maxillofacial Surgery of the U.H. «La Paz» over the last five years. The object of the study was to determine the frequency of these clinical symptoms in these patients, and to establish the best guidelines for the diagnosis, treatment and possible prevention of postoperative polyuria in future cases.

Material and method

We have revised the records of patients that underwent orthognathic surgery in our Service between 1997 and 2002.

Of the 172 cases operated, we have been able to gather reliable data from 118. In reoperated cases we have considered each surgical act as an independent case.

The average age was 20, and the age range varied between 15 and 57.

Of the 118 cases, 95 required bimaxillary surgery, and only 23 required monomaxillary surgery (16 upper maxilla and 7 mandible). These 23 patients made up of 13 women and 10 men, went from the operating room to the postoperative recovery unit (without passing through the intensive care or resuscitation units) for a few hours. From there they were taken directly to our hospital floor where diuresis was not strictly monitored, and as a result we have not been able to include these cases in our study. Therefore, of the 118 cases finally analysed the data proceeds from 95 cases.

The data studied is related to the surgery and to the period spent in the resuscitation or intensive care units. It was obtained by means of a revision of the anesthesia and progress records. We have collected the following data regarding the surgery: duration, diuresis, volume of liquids administered, type of maxillary osteotomy, type of mandibular osteotomy, maxillary repositioning and mandibular repositioning. From the period spent in the resuscitation or intensive care unit we have collected, over every 24 hour period, the data regarding the volume of liquids perfused, diuresis, natremia, serum potassium level, and in some cases urine density, urine osmolarity, urine sodium and urine potassium.

All patients were anesthetized by two anesthesiologists using a similar technique so as to exclude the influence of this factor.

We have considered polyuria as the internationally accepted criteria of diuresis in excess of 2 mL/hour, observed during the first 24 postoperative hours.


Most patients submitted to orthognathic surgery were young individuals as, although the age range was between 15 and 57, + nearly all of them were in the 20 to 23 age group.

59 patients of the 95 that passed through the postoperative resuscitation unit (34 women and 9 men) did not present polyuria. The remaining 36 patients developed early polyuria (Table 1) that varied between 2260 ml and 5835 ml of urine, with an average of 3286 ml of urine in the first 24 hours. All patients developed the polyuria during the 24 hours that followed the surgery, except one case that presented 2260 ml of urine on the first postoperative day, which increased to 3540 ml on the second.

These were simple polyureas that were not accompanied by ionic changes. The plasma values of sodium and potassium were maintained in all cases within normal limits (between 3.5 and 4.5 mmol/L potassium, and between 135 and 145 mmol/L sodium), except in one patient that had on his first day in the resuscitation a potassium value of 3.39 mmol/L, and another that on the second day in the resuscitation unit, had a 24 hour diuresis of 5890 ml with a sodium of 132.9 mmol/L. Both cases were resolved with adequate hydroelectrolytic replacement (Table 2).

The duration of these polyureas was self-limiting, and it was successfully treated in all cases with appropriate hydrolelectrolytic regulation. This was carried out by means of a protocol according to which a restriction of liquids during the acute stage was imposed, with half of the hourly diuresis being replaced with 5% serum glucose, and intranasal desmopressin (Minurin®) for refractive cases (only one in our series).

There were no complications of a greater magnitude. The patients with polyuria were brought to our hospital floor following a period in the resuscitation or intensive care unit of 18 to 72 hours. This was longer than the time spent by those patients without this problem, who abandoned the resuscitation or intensive care units during the first 24 hours of the postoperative period.


The results show how nearly 50% of our patients treated for dentofacial deformities with orthognathic surgery develop clinically evident polyuria during the postoperative period.

The differential diagnosis regarding the causes of this polyuria is of interest to us for two fundamental reasons:

1. The first is the possibility of finding a potentially treatable cause that could prevent its development and the consequential discomfort that it has for the patient, such as a longer period with a urethral catheter or the risk of dehydration.

2. The second is that, depending on the cause of the polyuria, the treatment is different. In this sense, a certain therapeutic approach that improves one type of polyuria can cause polyureas produced by other causes to become significantly worse.

This leads us to question the cause of the polyuria that develops in the postoperative period of our patients. Various possibilities have been put forward:

1. Water intoxication produced in the operating room.

2. Suppression of hypophyseal secretion of the antidiuretic hormone following facial osteotomies. Central diabetes insipidus is a complex hormonal disorder characterised by an excessive production of urine. It appears as a result of changes in the hypothalamo-hypophyseal axis that reduce the production of ADH. The most common etiologies are tumors and infections of the CNS, traumatisms or craniofacial surgery (it has also been described on a spinal level, but less frequently). ADH suppression could be produced by a transitory hypophyseal dysfunction as a result of the pituitary gland being jolted following a maxillary osteotomy.2,6-8

3. Salt wasting syndrome related to the inadequate excretion of atrial natriuretic peptide (ANP).1,2

In the differential diagnosis of polyureas, the first step is to determine urine density. If this is greater than 1005, it is most probably an osmotic polyuria, due either to hyperglycemia, or to hyperosmotic solutions having been administered (for example Rheomacrodex®).

If the urine density is less than 1005, the next stage is to calculate the corrected natremia according to the glycemia. For this we should apply the following formula:

Na(c) = Na(m) + [glycemia (mmol)-5]/ 3, where:

- Na(c) is the corrected glycemia
- Na(m) is the measured glycemia

A corrected natremia that is less than 137 would lead us to think that water excess was the cause of the polyuria. These cases respond well to fluid restriction. If a corrected natremia is greater than 142, the suspected diagnosis will be a true diabetes insipidus. Urine osmolarity less than 200 mOsm/kg would confirm the diagnosis. In these cases, water restriction is not efficient, and treatment with desmopressin is necessary. If this also were not effective, the cause of the diabetes insipidus would be nephrogenic and not central.

With regard to ANP, we should add that it is a peptide secreted by the atrium as a response to hypervolemia (detected through tension receptors in the atrial wall, that are stimulated physiologically by the atrial stretch). This has a diuretic effect that seeks to redress the volume balance in situations where there is volume excess. A hypothesis exists regarding the intermittent positive pressure-mechanical ventilation to which the patients are submitted during the surgery that could produce increased pressure in the atrium. This increase in pressure is captured by the receptors in its wall that activate, on being stimulated, the secretion of ANP, and this could increase the diuresis in a non-physiological manner. This theory, valid along general lines, does not however explain why we do not find polyuria in many other types of surgery in which patients are submitted to positive pressuremechanical ventilation.

Following discussions with endocrinologists and anesthesiologists in our hospital in the light of the data gathered, we do not believe that the settings described relate to true diabetes insipidus, as firstly the natremia constantly remains within normal limits, which is incompatible with an ADH deficiency. And, in second place, patients responded favourably to water restriction which, as we have just described, does not occur with true diabetes insipidus, where the kidney is incapable of concentrating urine despite the dehydration of the patient. Both sets of data would indicate a polyuria of a non-endocrine origin, that is to say, that the patient experienced an excessive intake of water during the surgery.

However, the type of anesthesia and the anesthetists are the same as those used in other of surgery where we work on facial bones and where polyuria has not been observed. This leads us to believe that an endocrine factor (ADH or ANP) does in fact play a role in its appearance.


This leaves the door open to future investigations to provide information as to the condition of the hypothalamushypophyseal axis, urine osmolarity and regulated natremia, which should seek a disturbance that will serve to guide us. In the mean time we should keep in mind the possibility that this [disorder] can occur, and we should supervise patients closely in order to carry out correct water regulation, especially now that there is a growing tendency to send patients prematurely to our hospital floor. Although patients presenting this disorder are infrequent and self-limiting, strict observation is required, as it is a potentially lethal situation. The cornerstone to diagnosis is a rigorous monitoring of fluids and electrolytes. Treatment consists in water restriction during the acute phase, and demeclocycline for refractory cases.


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