Hysteroscopic surgery: avoid the complication of hyponatraemic encephalopathy
Posted on May 29, 2008
Filed Under Knowledge Based, Uncategorized |
J. E. CARTER
Advanced Surgical Education Associates, and Women’s Health Center of South Orange County, Mission Viejo, CA, USA
Summary: Hysteroscopic surgery presents risks of four major complications: (1) hyponatraemic encephalopathy; (2) uterine perforation (either with or without bowel injury); (3) haemorrhage; (4) infection. To perform this procedure safely, the surgeon must be fully aware of the principles of: (1) fluid management; (2) electrosurgery; (3) bleeding control. The most severe complication which confronts the surgeon in hysteroscopic surgery is neurological sequelae from hyponatraemic encephalopathy. Premenopausal women are 26 times more likely to suffer neurologic sequelae from hyponatraemia as post-menopausal women or men. These women suffer permanent brain damage, paralysis and even death. To prevent this complication, premenopausal women should be transformed into post-menopausal women prior to the performance of a hysteroscopic operation using hyponatraemic fluids as distension media. This can be accomplished by giving GnRH agonists in sufficient quantity and for sufficient length of time to induce menopause. This paper presents a case reviewed by the author of a young women in whom this was not done and who suffered irreversible neurological consequences from hyponatraemia during a hysteroscopic resection of a small submucous myoma. In addition to the severe irreversible damage suffered by this previously healthy young woman, a jury awarded 24 million dollars in a judgement against the physician and the surgery centre involved in her care. The medical and legal consequences of complications of what should be a simple and safe procedure may in fact be unacceptable if precautions are not taken to protect patients from the consequences of hyponatraemic encephalopathy.
Keywords: hysteroscopic surgery, endometrial ablation, hysteroscopic myomectomy, hyponatraemia, encephalopathy
Case report: The author reviewed a case of a 27-year-old healthy female who complained to her physician of intermittent bleeding and spotting as well as prolonged periods and heavy bleeding with her periods. Without performing an ultrasound and after only two weeks of attempted therapy with oral contraceptives, the surgeon caring for this women scheduled an out-patient diagnostic hysteroscopy.
The diagnostic hysteroscopy was performed with a high flow, high pressure pump approved only for laparoscopic use. The fluid used was a mixture of 10% Hyscon by volume in normal saline. Approximately 800 cm3 of this fluid were used in a few minutes. A submucous myoma was found during the hysteroscopy which was performed under general anaesthesia.
The surgeon, despite lack of consent for an operative procedure, proceeded with a hysteroscopic myoma resection. For this procedure, the fluid was changed to sterile water. Approximately 1 litre of this fluid was infused in a few minutes. No accurate fluid monitoring was performed. The patient became bradycardic,
hypertensive followed by hypotensive, developed pulmonary oedema, and the pulse oximeter reading decreased. The QRS complex widened and the patient then had a seizure and cardiac arrest.
A CT scan performed after the event demonstrated cerebral oedema. She is currently blind, deaf and quadraplegic, but aware of her surroundings. A jury awarded 24 million dollars to her for medical expenses, pain and suffering.
Introduction: Hysteroscopic surgery is rapidly replacing hysterectomy for the indications of symptomatic uterine pathology [1-8] (polyps, intracavitary and submucous myomas), as well as for dysfunctional uterine bleeding unresponsive to hormone therapy [9].
This procedure is performed either with Nd:YAG laser [10-18] or with electrocautery by either resection [19-27] or ‘roller ball’ technique [28-31]. The early procedures of both hysteroscopic fibroid treatment and endometrial ablation were performed using the Nd:YAG laser and therefore the procedure was restricted to those practitioners comfortable with this energy modality. In addition, the procedure was performed with normal saline isotonic solutions since the Nd:YAG laser functions well in any type of fluid environment. As a result, problems that can occur with the use of solutions suitable for electrocoagulation (solutions which contain no sodium) did not occur. Even with the use of the resectoscope in the early cases in which it was introduced, there were no reports of significant problems with the procedure which was still performed only by a very limited group of practitioners.
With the introduction of the ‘roller ball’ by Lin [28], Vancaille [29] and Townsend [30], the practice of endometrial ablation became more widespread. In 1993 a report on endometrial ablation complicated by fatal hyponatraemic encephalopathy was published. Four healthy women who underwent elective endometrial ablation for dysfunctional bleeding experienced hyponatraemia. Three of them recovered. One suffered grand mal seizures and respiratory arrest and then died [32].
In two of the patients hyponatraemic encephalopathy was diagnosed intraoperatively because of tremulousness and either hypothermia or hypoxaemia. In the other two patients the diagnosis was made post-operatively because of headache, nausea, emesis and, in one of these patients, respiratory arrest [32].
The possibility exists that significant under-reporting of this severe complication of endometrial ablation is occurring. The American Association of Gynecologic Laparoscopists 1993 Membership Survey on operative hysteroscopy reported a 2 per 1000 rate of water intoxication and pulmonary oedema and no deaths for that year [33].
Four cases of severe hyponatraemia occurring during operative hysteroscopy and resulting in a 50% death rate were presented in the literature during the same year [34]. In these cases glycine 1.5% or sorbitol 3% was used for uterine irrigation. These reports of complications triggered an editorial by one of the leading practitioners of hysteroscopic surgery which warned that, ‘without exception, every variety of distention media can be associated with serious side effects especially if the uterine wall is disrupted. When such circumstances exist, the medium is transmitted via the uterine veins into the systemic venous circulation and subsequently ends up in the right atrium in the pulmonary vascular tree. Complications, such as pulmonary edema, hyponatraemia, and bleeding diatheses, are dangerous. It can be expected to happen with increasing frequency. A complacent attitude on inaccurately and casually approximating fluid deficits would lead to adversity for the patient as well as the attending physician’ [35].
Post-operative hyponatraemia has become a significant medical legal risk and the implications of this problem were brought forward by a major malpractice insurance company which published a risk management update on this topic [36]. In this report it was indicated that hyponatraemia can be associated with permanent brain damage or death and that premenopausal women are 26 times more likely to die or have permanent brain damage from hyponatraemic encephalopathy than post-menopausal women [37-39].
Endometrial ablation [32], hysteroscopy [40] and transurethral resection of the prostate [41] have been linked with hyponatraemia because of intraoperative absorption of non-electrolyte irrigant fluid.
Discussion: Hyponatraemic encephalopathy
Hyponatraemia is defined as serum sodium concentrations <130 meqll. Normal serum sodium is 135-142 mEq/l.
Hypotonicity is defined as a serum osmolality level of <280 mosm/kg.
Isotonicity is defined as an osmolality of 280-295 mosm/kg.
Hypertonicity is defined as an osmolality of >295 mosm/kg.
As early as 1986 recognition was given to the severity of the problem of hyponatraemic encephalopathy [42]. In this study, 27% of the patients died, 13% had limb paralysis, and 60% were left in a persistent vegetative state after elective surgery was performed in 15 previously healthy women who developed hyponatraemia [42].
Hyperglycaemic hyponatraemia occurs when the blood glucose level is greater than 300 mg/dl. Each 100 mg/dl increment in the blood glucose value produces a 2 mEq/l decrement in the plasma sodium concentration. 4.4% of patients undergoing operative procedures develop hyponatraemia and 21% of these occur because of the water shift induced by hyperglycaemia [43].
Antidiuretic hormone is increased in many patients during or after surgery and can result in dilutional hyponatraemia. In the syndrome of inappropriate ADH secretion (SIADH), release of ADH occurs without osmolality-dependent or volume-dependent physiologic stimulation. The causes of SIADH are disorders that affect the central nervous system - structural, metabolic, psychotic or pharmacologic - or the lungs. ADH levels are increased during surgery or as a result of pain [44].
In addition, as shown in Table 1, many medications increase ADH production. SIADH is characterized by hyponatraemia, decreased osmolality (<280 mosm/kg) with inappropriately increased urine osmolality (>200 mosm! kg) with normal thyroid and adrenal function.
Table 1: Causes of drug-induced SIADH
| Increased ADH production | Potentiated ADH action | |
| AntidepressantsAmitriptylineClomipramine
Desipramine Imipramine Lofepramine Monoamine oxidase inhibitors Nomifensine Fluoxetine |
AntineoplasticsCyclophosphamideVincristine
Vinblastine Carbamazepine Clofibrate Neuroleptics Thiothixene Thioridazine Fluphenazine Haloperidol Trifluoperazine |
Carbamazepine,oxcarbazepineChiorpropamide,
tolbutamide Cyclophosphamide NSAIDs Somatostatin and analogues |
Factors related to development of hyponatraemic encephalopathy
The relative risk of dying or developing permanent brain damage from hyponatraemia is 26 times as great for premenopausal women as for post-menopausal women [38]. Only 2% of post-menopausal women who were hyponatraemic developed permanent sequelae whereas 60% of the premenopausal women who developed hyponatraemia developed permanent sequelae of encephalopathy. Menstruant women are at high risk of death or permanent brain damage from even modest post-operative hyponatraemia (serum sodium level 120-132 mmoVl) [38].
The reason for a female predilection to brain damage from hyponatraemia is not clear. The efflux of osmotically active cations (primarily potassium) and a gain of water acts to lower the intracellular osmolality of the brain in the presence of hyponatraemia. The rapidity of the process may ultimately determine survival
[32]. The active component of potassium release is mediated by sodium-potassium ATPase. This is apparently inhibited by some female sex hormones. It has been demonstrated that progesterone and certain of its derivatives can inhibit this enzyme in several tissues [45].
GnRH agonists create a post-menopausal state in premenopausal women. Serum oestradiol levels decreased to menopausal levels 1 month after therapy with injection of 3.75mg depot leuprolide acetate (Lupron, Tap Pharmaceuticals, Deerfield, IL, USA) in 96 women in whom it was administered. The mean level of oestradiol was 22 pg/mI, with a range of 12-34pg/ml [46]. Men frequently develop more severe hyponatraemia (serum sodium <110 mmol/l) after excess fluid absorption during transurethral prostate resection (TURP) [47]. However, in men the relative risk of brain damage from the hyponatraemia is less than 4% that of menstruant women [38].
Trans-uterine and peritoneal absorption of uterine distension media whether glycine or sorbitol can occur. Serious neurologic problems of acute hyponatraemia appear to be gender related. As noted, there is a predominance of female susceptibility to cerebral oedema [38, 39, 42, 48].
The choice of distending medium influences the risk of cerebral oedema. The osmolality of serum is 285 mosm/l. Three per cent sorbitol has an osmolality of 178 mosm/l, 1.5% glycine 200 mosm/l. Five per cent mannitol osmolality at 280 mosm/l is the safest non-conductive agent available to distend the uterus. Mannitol is rapidly excreted by the kidney resulting in a rapid osmotic diuresis. The rapid production of dilute urine may be the first sign of fluid overload with the use of 5% mannitol [32].
A prospective randomized study was performed to determine the effect of intrauterine pressure on medium absorption during endometrial ablation with the Nd:YAG laser. Two pump systems were compared while continuously monitoring intrauterine pressure. The mean fluid absorption with a constant flow pump was
five times higher than with a pressure-limited pump [49].
Patients who underwent deep myometrial injury during ablation absorbed significant amounts of distension fluid regardless of optimal control of intrauterine pressure [50].
Relation of hyponatraemia to permanent brain damage
Hyponatraemic encephalopathy is a result of the osmotic imbalance between extracellular fluid and brain cells which leads to a net movement of water into the brain and results in cerebral oedema.
If hyponatraemia persists, the brain swelling will exert pressure against the rigid skull and may subsequently lead to brain pressure necrosis. When the brain expands by more than approximately 5% of its volume, cerebral herniation will ensue unless appropriate treatment is promptly instituted [51].
Studies have demonstrated that several steroid and peptide hormones can cause water movement within the ONS in the absence of a low serum sodium concentration [53].
These include sex hormones (such as progesterone, oestrogen and testosterone) and vaso-active neuropeptides including ADH, atrial natriuretic peptide and angiotensin [53]. When ‘hyponatraemia occurs the brain has only two basic responses: adaptation by loss of osmotically active solute (primarily sodium and potassium) and gain in water [53]. A gain in water will lead to brain oedema, cerebral damage and possibly herniation and death. Solute extrusion on the other hand can minimize or altogether prevent cerebral injury associated with hypo-osmolar states.
Hyponatraemic encephalopathy involves an imbalance between selective loss of solute versus gain of water. The balance between loss of solute versus gain of water effectively determines survival of the organism.
The mechanism of loss of cation from brain cells in hyponatraemia is not totally understood but it has an active and passive component. In animals made acutely hyponatraemic (over 1-2 h), brain water content is substantially elevated but the electrolyte content (milliequivalents per kg of dry weight) is only minimally decreased [48, 53].
The presenting symptoms of hyponatraemic encephalopathy can include opisthotonos, respiratory depression, impaired response to verbal and/or painful stimuli, bizarre behaviour, incontinence of urine or faeces, visual or auditory hallucinations, lethargy, decorticate or decerebrate posturing, and seizure
activity. Respiratory arrest, fixed, dilated pupils and abnormal temperature regulation may also develop [54].
Hyponatraemic encephalopathy demonstrates a clear predilection for women who are of reproductive age (13- 50 years). Major determinants of brain damage in hyponatraemia are the age and sex of the patient. Most patients with symptomatic hyponatraemia (serum sodium concentration below 120 mEq/I) in whom permanent neurologic damage did not develop were men or older women, whereas those who died or suffered permanent brain damage were younger women [37-39].
Recognition and treatment of hyponatraemic encephalopathy
In the awake patient the symptoms and signs of hyponatraemia include the following symptoms: apprehension, disorientation, irritability, twitching, nausea, vomiting and shortness of breath; and the following signs: bradycardia, hypertension, anaemia, jaundice, cyanosis, altered sensorium, ECG changes and seizures. When severe hyponatraemia is associated with hypo-osmolality, the condition can lead to significant central nervous system injury with a mortality rate of 33-86% [55].
In patients undergoing general anaesthesia during endometrial ablation, the possibility of hypo-osmolality/hyponatraemia should be suspected if there is (1) decrease in body temperature, (2) decrease in oxygen saturation, (3) tremulousness, or (4) dilated pupils (indicative of increased brain pressure on third nerve). Early and appropriate therapy for the hyponatraemia is indicated before respiratory insufficiency occurs in order to reduce morbidity and mortality [32].
Rapid treatment with hypertonic saline administered at a rate of >1 mmol V1 h1 should be reserved for acute cases since the treatment itself can produce central pontine myelinolysis if carried out too rapidly. Sodium levels <120 mmoVl occurring acutely are considered significantly depressed to warrant immediate treatment. Correction should be preceded by administration of intravenous furosemide to prevent circulatory overload. Hypertonic sodium chloride is administered as a 3-5% solution with the goal of increasing the
serum sodium concentration to approximately 125-135 mmol/l within 24 h. The rate of hypertonic saline solution should approximate 1.3-1.6 mmol V1 h1 [37].
In acute water intoxication the presenting symptoms, seizures and/or respiratory arrests, are often quite dramatic. Therapy may be unlikely to produce a good outcome. Acute hyponatraemia is more common after hysteroscopic surgery in which hypotonic solutions are being infused into the uterus. Treatment begun after acute symptoms arise is often associated with mortality and neurologic morbidity.
The goals of therapy for acute hyponatraemia are to reduce brain water and to increase extracellular fluid sodium concentration to the degree necessary to maintain normal respiration and keep the patient seizure-free and alert. Nor should the absolute change in serum sodium concentration be >25 mEq/I during the
first 48 h of treatment. The total correction of acute hyponatraemia should take place over 48 h. Sodium repletion should be discontinued when the following occur:
1. The patient becomes completely asymptomatic (seizure free, alert, clinical conditions stable),
2. Serum sodium concentration is increased by 20- 2smeq/l, or
3. Serum sodium level has risen to between 122 and 125 mEq/l and the patient is stable.
Findings in animal studies demonstrate that an osmotic gradient of at least 30 mosm/kg H20 between the plasma and the brain appears to be necessary to promote an acute loss of or net gain in brain water [56]. The optimal range of correction of symptomatic hyponatraemia is between 14 and 25 mEq/l during the first 24 h. Grades of changes lower or higher than that range are associated with significant mortality or brain lesions [37, 56, 57].
The real issue in the treatment of hyponatraemia is not the rate of repletion but rather the rate of diagnosis. When the diagnosis is made promptly and appropriate treatment begun in a timely fashion before respiratory arrest can occur, morbidity and mortality can be minimized [54].
Hypertonic saline solutions are usually infused, often in conjunction with a loop diuretic such as furosemide. Infusions of isotonic solutions are useful until completion of basic laboratory and clinical examinations because isotonic saline solutions are in fact hypertonic to the patient with hypo-osmolarity.
Furosemide causes diuresis of water and excess of solute when given acutely and can be used to accelerate water excretion [57].
Symptomatic hyponatraemia should be managed with hypertonic saline (usually 3%) and infused at a rate designed to increase the level by 1 mEq/I/h. These infusions should continue until the patient becomes asymptomatic or serum sodium level of 120 mEq/l is obtained, at which point the saline infusions should be
discontinued. Serum sodium levels should be checked every 2 h. Cerebral demyelinating lesions can develop if the serum sodium level is over-corrected so the serum level should not be elevated acutely above 120 mEq/I. The serum sodium should not be elevated by more than 25 mEq/l during the first 48 h of therapy
[57].
In symptomatic hyponatraemia associated with SIADH, serum sodium concentrations should be raised at this rate by using a combination of 3% saline infusions and intravenous furosemide (40 mg) [57].
Example of calculation of infusion rate for correction of hyponatraemia [57]
1. Estimate the total body water (TBW) as 48% of the weight in kg.
2. Calculate the sodium deficit by subtracting the patient’s serum sodium from the goal of the correction (120 mEq/l) and multiply the result by the total body water in litres.
3. Assume a rate of correction of 1 mEq/l/h so the number of hours of infusion will equal 120 minus the patient’s serum sodium concentration measured in milliequivalents.
4. Determine the infusion rate by dividing the sodium deficit in milliequivalents by the number of hours.
5. To calculate the infusion rate in ml per h, multiply the infusion rate measured as milliequivalents per h by 1000 and then divide by 514, which is the number of milliequivalents per litre in 3% saline.
Example: 50kg female with serum sodium of 105 mEq/l
1. Total body water is one half body weight or 25 litres.
2. Sodium deficit (120 mEq/l - 105 mEq/l) x (25 litres) 375 mEq.
3. At a rate of 1 mEq/l/h, the 15 mEq/l difference could be accomplished in 15h.
4. Sodium should be administered at 375 mEq/ 15h=25meq/h; using 3% saline (5l4meq/l) the infusion rate equals 25 mEq/h x 1000 ml) + 514 mEq = 49 mI/h
5. Thus 49 mI/h of 3% saline should be administered for 15 h.
Conclusion and recommendations for operative hysteroscopy
1 Infusion fluid- Infusion fluid of 5% mannitol should be used because the osmolality of 5% mannitol at 280 mosm/kg most closely approximates the osmolality of serum [58].
2 Anaesthesia - Regional anaesthesia should be used (epidural or spinal) because the earliest symptoms and signs of hyponatraemic encephalopathy include nausea and vomiting, agitation, irritability, delirium, weakness and seizures, which can be detected by the anaesthesiologist.
3 Intravenous fluid - All intravenous fluids should be isotonic, such as normal saline or lactated Ringer’s, and given at a ‘To keep open rate’.
4 Infusion pressure - Infusion pressure should be less than the mean arterial pressure [(systolic pressure plus two times the diastolic pressure) divided by three]. Avoid pressures over 80 mmHg intrauterine [59]. This is equivalent to approximately 1 m above the patient’s pelvis. (To compute gravity pressure, recall that mercury is approximately 14 times as dense as water. One metre of height above the patient’s pelvis is 1000mm of water pressure which divided by 14 is equivalent to 70 mm of mercury pressure. Suspending the bag of irrigant fluid 3 feet (1 m) above the patient’s pelvis will give the equivalent of 70mm of pressure at the uterus. To compute the millimetres of mercury pressure for any other height, simply divide the height that the bag is above the patient in millimetres of mercury by 14 and you will have the millimetres of mercury pressure at the uterus.)
5 Menstrual status - GnRH agonist should be given until the patient is post-menopausal by evaluation of hormone levels [60]. Patients who are premenopausal are 26 times more at risk of suffering permanent neurologic deficits or death from hyponatraemia as women who are post-menopausal. Oestradiol levels should be checked prior to performance of the procedure to ensure post-menopausal state.
6 Fluid monitoring - Fluids must be monitored on a frequent basis approximating every 5 mm. Significant fluid intravasation can occur through an open venous channel in a 5 mm period which can result in a very rapid change is serum sodium and result in severe dilutional hyponatraemia and encephalopathy. More precise methods of monitoring vascular uptake of hysteroscopic distension media are required. Simply keeping track of fluid intake and output is not sufficient. Each patient should be assigned a maximum allowable fluid absorption (MAFA) [61]. At a MAFA of 17.6m1/kg a fall in serum sodium concentration of more than 10 mEq/l does not occur [61].
7 Vasopressin - Vasopressin (Pitressin) has risks as it adds exogenous antidiuretic hormone to patients who are at risk of developing inappropriate secretion of anti-diuretic hormone which can result in post-operative or intraoperative dilutional hyponatraemia.
8 Sodium levels - Serum sodium levels should be measured preoperatively. Intraoperative sodium should be obtained if fluid loss of more than 500 ml is suspected. Post-operative serum sodium should be monitored.
9 Diuretics - Furosemide should be administered if fluid absorption of more than 500 cm3 is suspected.
10 Medications - All medications that can contribute to inappropriate secretion of antidiuretic hormone (SIADH) should be discontinued prior to the procedure.
11 Time of procedure - The procedure must be performed expeditiously (in less than 1 h if at all possible) as fluid absorption increases with the length of time of the procedure.
12 Preparation of endometrial lining - GnRH agonists should be used to prepare the lining of the uterus. This results in a thinner lining to treat and therefore results in a more uniform treatment and a shorter procedure which improves the safety of the procedure.
13 Preparation of fibroids - GnRH agonist or danazol should be given prior to hysteroscopic resection of submucous and intracavitary myomata to reduce the size of the myomas and to protect against dilutional hyponatraemia [62].
14 Technique - The technique to perform operative hysteroscopy safely must be designed to avoid the most devastating consequence [63]. The most devastating consequences that can occur from operative hysteroscopy are the neurologic sequelae (which can include death) from hyponatraemic encephalopathy.
15 Bleeder coagulation - Manipulate the flow valve on the inlet for the hysteroscope in order to reduce pressure to see individual bleeders. Cauterize these bleeders as the procedure is carried out. This will avoid pushing fluid in through vascular channels as the procedure is carried out.
Conclusion: The first rule of the physician is to ‘do no harm’. To expose young, healthy women to a risk of neurologic deficit for treatment of benign disease is unacceptable especially if techniques exist to reduce this risk. The simple action of transforming a premenopausal woman into a post-menopausal woman reduces her risk of neurologic sequelae from hyponatraemia 26 times.
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For original publication, please see: Carter JE. Hysteroscopic surgery-avoid the complication of hyponatraemic encephalopathy. Min Invas Ther & Allied Technol 1997: 6: 241-248
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