Fluid Shift in Bilateral Varicose Vein Surgery

Dr. Vasanthi Vidyasagaran*

Department of Anaesthesiology, Kauvery Hospital, Chennai, Tamilnadu, India

*Correspondence: Vasanthi.vidyasagaran@gmail.com

Dr. Vasanthy Vidyasagaran Muralidharan


A 70-year-old man was posted for bilateral varicose vein surgery (vein stripping and saphenous-femoral ligation). His veins were huge and tortuous. He had a history of MI 5 years ago, reasonably stable, on coronary vasodilators.

All blood Investigations were within normal limits. ECG showed old anterior wall MI. Echo showed mild LV dysfunction, with an ejection fraction of 40%

On Examination BP 130/80 mm Hg, HR 76 beats/min, normal sinus rhythm, chest was clear, no added murmurs. Patient was taken up under spinal anaesthesia, ASA 3 status. Preoperatively he was fasted for six hours, started receiving IV fluids at 80ml/hr 5 hours prior to the scheduled time of surgery.

Standard monitoring was applied, spinal anaesthesia was given in the right lateral position with 3 ml 0.5% heavy Bupivacaine and 25 mcg Fentanyl at L3/L4 level. Fifteen minutes later his BP began to drop to 80/50 mm Hg. Ephedrine 6mg bolus was given thrice until BP stabilized at 110/70 mm Hg. Further 2 litres of intravenous crystalloids were given during that time. Surgery lasted for three hours, with no further events.

On second postoperative day, the patient complained of headache. Suspecting post dural puncture headache, the head was placed flat on the bed without a pillow, his legs were raised and a further 2 litres of IV fluids were administered. Two hours later, he started to complain of difficulty in breathing, and was getting restless.

He had tachycardia of 120/min, BP 90/50 mm Hg, and sao2 dropped to 92%. Chest examination revealed basal crepitation, and presence of pulmonary oedema was confirmed by chest X-ray. Patient was placed head up, IV Lasix 40 mg given and fluids stopped. Oxygen was administered through CPAP mask. Patient recovered well.


After spinal anaesthesia, vasodilatation occurs and there is a drop-in blood pressure. Hypotension gets exaggerated when both legs have varicose veins. At the end of the procedure when bandage is applied there could be an increase in venous return precipitating fluid overload, particularly in patients who have been administered additional IV fluids to combat the spinal hypotension. I have always noticed an increase of blood pressure of up to at least 20 to 30 mm at the end of the procedure when elastocrepe bandage is applied (observations done in 90 patients). Vasopressors must also be used with caution and reservation, constantly monitoring the haemodynamic status. Increasing the rate and volume of intravenous crystalloids is not ideal in these situations. Whereas in the above scenario, nearly 8 litres of IV fluids were administered within 24 hours, resulting in pulmonary oedema in an elderly patient with an existing cardiac disease, though the myocardial infarction had occurred several years ago.

In patients with significant bilateral varicose veins, it may be preferable to operate one limb at a time, supporting the other limb on a lithotomy rod.

There may sometimes be brisk blood loss during bilateral surgery that needs to be replaced with packed cells, rather than resort to replacement with fluids.

In patients with peripheral vascular disease, oedema may coexist due to venous incompetency. At the end of surgery, this extra vascular fluid may enter intravascular space and precipitate fluid overload. In the perioperative period, there is also a rise in antidiuretic hormone. Therefore, caution must be exercised in fluid management, particularly in an elderly patient, who has suffered an MI and has a low EF. In young patients with good cardio respiratory reserve this variation may not precipitate any untoward event as it may get well compensated.

In this case, a combination of factors like excess fluid administration, reduced renal capacity and fluid shift between vascular compartments, along with MI and low EF contributed to pulmonary oedema.


When minimally invasive varicose vein surgeries are performed, including radiofrequency ablation, use of femoral nerve block with intravenous sedation is the current preferred practice, as opposed to spinal anaesthesia.


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[2].       Hagerstwon, Fluid imbalances in Portable Fluids and Electrolytes. Lippincott Williams and Wilkins. 2007

[3].       Sharon L Lewis et al.Medical- Surgical nursing 2014. (9th edition) Assessment and Management of clinical problems.

POST-OPERATIVE  – Chapter 10

Gestational Diabetes Insipidus

A 24-year-old, primiparous woman was admitted with history of sudden increase in blood pressure over past 48 hours. She was feeling very tired and dehydrated. She was medically treated with antihypertensive drugs – Nifedipine & Labetalol. Her liver function tests, coagulation profile, and other blood investigations including thyroid function tests were normal. She was 38 weeks pregnant. 12 hours into admission, she had decreased foetal movements. She was taken up for emergency LSCS under spinal anaesthesia.

The surgery was completed uneventfully and the patient was shifted to the ward. However, patient continuously complained of being thirsty, and a dry tongue. Intravenous fluids were given as bolus and maintenance rate was increased. In recovery, it was noticed that her systolic blood pressure remained around 80-90 mm Hg even after recovery from spinal anaesthesia. However, her urine bag was constantly filling up with dilute urine of over a litre in 3 hours. Oral fluids were commenced to help hydration. Intravenous fluid replacement to combat the volume of urine loss was administered. She started complaining of headache, and getting increasingly tired.

Suspecting immediate postoperative haemorrhage, the surgeons checked the abdomen and pelvis. There were no signs of bleeding. Bed side ultrasound revealed no bleed. The type of headache did not fit into picture of post-dural puncture headache. Her glucose levels were checked and were normal. Blood sample was sent to check the liver function tests, blood sugar and serum sodium and potassium levels. At that point of time the differential diagnosis included:

  • Unrevealed PPH – not entirely ruled out
  • Preeclampsia progressing to decompensated cardiac function
  • Post-dural puncture headache
  • Gestational Diabetes Insipidus


During the entire course of time, patient’s urine output was high and vasopressors were required to maintain mean arterial pressure at 60-70 mm Hg. Her blood sugar, liver function tests and coagulation profile were normal. Serum sodium was 158 mEq/L. Patient’s urine sample was sent to check for osmolality to confirm diagnosis. Once the diagnosis became clear as Gestational Diabetes Insipidus, patient was administered nasal spray of Desmopressin, DDAVP. Adequate volume replacement was continued. Within 4 hours, patient began to feel better and her symptoms began to recede. DI may be a pre-existing disease or may have been precipitated by the pregnancy and/or surgery (gestational DI).


Gestational diabetes insipidus is a rare complication of pregnancy. It is thought to be a result of increased degradation of Arginine Vasopressin by Vasopressinase produced by the placenta. This enzyme may be detected from 7th week of gestation, increasing to maximum by term and decreasing to normal by 6 weeks postpartum. This form of diabetes insipidus may be associated with increased complications of pregnancy, including preeclampsia and acute fatty liver of pregnancy. Some women may go clinically undetected, but some may have significant symptoms and immediate treatment is warranted, though clinching and confirming the diagnosis is difficult.

Treatment must include synthetic analogue of Vasopressin 1-Deamino-8-D-Arginine Vasopressin (Desmopressin Acetate) DDAVP, which is not metabolized by this enzyme. High index of suspicion would help diagnose this condition early and commence treatment before patient deteriorates.

DI can be the result of several other factors including:

  • Neurogenic: Deficit in the secretion of hypothalamus-hypophysis ADH
  • Nephrogenic: Renal tubular insensitivity to ADH
  • Psychogenic
  • Gestational

Management of central diabetes insipidus and transient diabetes insipidus of pregnancy can be achieved using DDAVP, a vasopressin analogue.

Nephrogenic diabetes insipidus is typically resistant to both DDAVP and Vasopressin

Hence underlying causes should be addressed. DDAVP is also preferable for use in antenatal women with preeclampsia because of its limited effect on vascular tone. Risk of reduced quantity of amniotic fluid has been quoted. Hydrochlorothiazide has been tried as second line with caution, due to risk of foetal hypoglycaemia and neonatal DI. DDAVP is secreted in mother’s milk in very small quantities, but poses little risk of fluid and electrolyte disorders in the new born.

Clinicians caring for pregnant women must be aware of this rare condition and diagnose it without delay to prevent any major complication.

Unexpected complications arise in the peripartum period

In this context,

I would also like to mention an interesting case of postpartum PIH. This was a young 24-year primigravida who had no antenatal medical history. All her investigations were normal, except for platelet count which was 80,000 at term. She had no complaints. Blood pressure was normal during her visits. She insisted on having an epidural for labour, in spite of explaining the risks involved with a low platelet count. Epidural was given since a count of 80,000 was not an absolute contraindication. It was uneventful and she delivered within four hours. As she was about to be shifted to the ward, she complained of severe headache and epigastric pain. BP shot upto180/118.she was very restless. Having given the epidural an intra cerebral bleed was a concern. Anti-hypertensives were given, but she responded only to magnesium sulphate. CT of the brain was normal. This was an unusual presentation of PIH, in the immediate postpartum period. Diagnosis was tricky because epidural was given with a low platelet count.


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