PRINCIPLES OF SURGERYFLUID AND ELECTROLYTE BALANCEPART 1: DISORDERS OF WATER AND SALT BALANCEJanuary 2010

Dr. Bob Richardson, Toronto General Hospital

Objectives (1)

1. Understand how humans maintain water balance

Role of ADH and thirst

2. Understand the role of sodium in body fluid homeostasis

Manifestations of sodium depletion

Objectives (2)

3. Know the mechanisms for postoperative hyponatremia

How to prevent it How to treat it

4. Know some of the literature on perioperative IV fluid therapy

5. Understand the mechanisms and treatment of surgically induced diabetes insipidus and hypernatremia

Case 1: 84 year old woman admitted for knee replacement. On thiazide diuretic for hypertension. Preoperative serum sodium 134 mmol/L (135-145). Postoperatively had frequent vomiting. Given 6 litres of 5% dextrose in saline for 2 days (i.e. 2/3-1/3 at 125 ml/h). After 48 hours became comatose, serum sodium was 115 mmol/L. Sodium concentration was corrected over 5 days but patient was left with permanent cognitive deficit.(Reported in BMJ 1999)

Question 1

She developed hyponatremia because she received:

A. Too much IV fluidB. Too much of the wrong IV fluidC. The wrong IV fluidD. Hydrochlorthiazide

Question 2

How should she have been treated after 48 h?

A. Water restrictionB. Isotonic salineC. Hypertonic salineD. Hypertonic saline + furosemide

Water Physiology

What protects us from hyponatremia or hypernatremia?

PHYSIOLOGY OF ADH AND WATER

Q: How would you make someone hyponatremic?

A: Give ___________________ and ________________________

ADH (vasopressin) causes collecting duct to reabsorb water

HYPONATREMIA = WATER EXCESS (relative to sodium)

Usually need water intake and ADH action to get hyponatremic

waterADH

Q: What prevents normals from developing hyponatremia?

A: suppress pituitary secretion of ADH

Allows the kidney to excrete large volumes of hypotonic fluid

In young healthy adults, in the absence of ADH, urine flow could be close to 1 L/h with an osmolality < 100 mosmol/kg)

Normal ADH physiology

ADH is secreted in response to an increasing serum sodium concentration

Exhibits a threshold and a slope: normal threshold is about 135 mmol/L below this value for serum sodium, ADH

should be totally suppressed. Most common reason for hyponatremia

= failure to suppress ADH when the serum sodium is < 135 mmol/L

ADH vs Serum Sodium:Threshold and Slope

0

1

2

3

4

5

6

7

8

120 125 130 135 140 145 150 155

Serum Na

AD

H

Thirst

Q: What prevents normals from developing hypernatremia even when fluid losses are high?

A: Thirst Drinking water lowers serum sodium

concentration back toward normal. Commonest cause of hypernatremia is

failure to drink fluid when water depleted. Note that increased ADH during

hypernatremia prevents excessive urine loss of water but does not replace water deficits.

Water PathophysiologyHow do things go wrong?

HYPONATREMIA Non-osmotic stimulation of ADH Reduced effective circulating volume Nausea Pain, psychological stress Pregnancy Drugs Cortisol deficiency, hypothyroidism Surgery Tumours (SCLC), intracranial disorders,

intrathoracic disorders (SIADH)

EFFECTIVE CIRCULATING VOLUME

Definition: the adequacy of arterial filling; depends on cardiac output and peripheral vascular resistance. Reduced when:

Cardiac output is reduced ( low intravascular volume or cardiac failure)

Peripheral arterial vasodilatation which is not matched by an equivalent increase in cardiac output (cirrhosis with ascites, distributive shock)

Characteristics of Low Effective Circulating Volume

low BP, postural fall in BP, low JVP signs of CHF: edema, pulmonary

edema, JVP ascites, edema tachycardia renin, angiotensin II, aldosterone,

noradrenaline, adrenaline, cortisol and ADH

ADH and Effective Circulating Volume ADH = vasopressin Important regulator of peripheral

vascular resistance Not surprising that ADH secretion is

stimulated by low ECV Primarily baroreceptor (carotid

sinus to brain stem to hypothalamus)

Kidney response to low effective circulating volume

low sodium excretion and low urinary sodium concentration (< 20 mmol/L)

low urine flow with concentrated urine (osmolality > 500 mosmol/kg)

may be low GFR with high creatinine

What factors could increase ADH levels in the perioperative state?

1. Reduced effective circulating volume

2. Nausea (surgery, narcotics)3. Pain, stress4. Surgery itself5. Ectopic secretion by tumours (SCLC)6. Release from damage to

hypothalamus, posterior pituitary

Why Reduced Effective Circulating Volume? Sodium loss: vomiting, ileus,

pancreatitis, NG suction, ileostomy, bile drainage, hemorrhage, diarrhea

congestive heart failure (MI, tamponade, arrhythmia)

cirrhosis/ascites sepsis (vasodilatation) epidural anesthesia

Effect of Surgery on ADH Secretion

ADH increases from 2 uU/ml to 25 uU/ml after manipulation of viscera during cholecystectomy.

ADH levels stay elevated following most types of surgery for 1.5 to 4 days

Abdominal and cardiothoracic surgery stimulate ADH more than others

ADH levels > 5-10 cause a maximally concentrated urine

Relationship of Sodium and Hyponatremia Why does sodium loss cause

hyponatremia? Even isotonic sodium loss can lead to

hyponatremia Loss of isotonic sodium (diarrhea,

burns, pancreatitis etc.) lowers effective circulating volume: ↑ ADH

If hypotonic fluid is given, water is retained - hyponatremia

POSTOPERATIVE HYPONATREMIA

CAUSE: stimulation of ADH secretion by surgery (or other factors) with use of either hypotonic fluid intravenously, or excessive amounts of isotonic fluid.

Patients at greatest risk are women and elderly, probably because they have smaller initial total body water due to low body weight and higher body fat

Incidence of Postoperative Hyponatremia

About 3-5% about one half have normal effective circulating volume

about one quarter have edema state

the rest are hypovolemic or have renal failure

Complications of Hyponatremia Acute severe hyponatremia (serum

sodium < 120 mM developing in less than 48 hours) causes brain cell swelling coma, seizures, hypoxia, death

Chronic hyponatremia usually asymptomatic unless very severe (< 110 mM) Brain volume can adapt to normal with chronic hyponatremia

Rapid correction of chronic severe hyponatremia may cause myelinolysis of brain resulting in severe irreversible brain injury

Case 1: 84 year old woman admitted for knee replacement. On thiazide diuretic for hypertension. Preoperative serum sodium 134 mmol/L (135-145). Postoperatively had frequent vomiting. Given 6 litres of 5% dextrose in saline for 2 days (i.e. 2/3-1/3 at 125 ml/h). After 48 hours became comatose, serum sodium was 115 mmol/L. Sodium concentration was corrected over 5 days but patient was left with permanent cognitive deficit.(Reported in BMJ 1999)

Why Did This Happen? ADH from low ECFV, nausea,

surgery Thiazides impair free water

excretion Excessive amount of dilute fluid Small elderly female Probably low GFR

Question 1

She developed hyponatremia because she received:

A. Too much IV fluidB. Too much of the wrong IV fluidC. The wrong IV fluidD. Hydrochlorthiazide

Question 1

She developed hyponatremia because she received:

A. Too much IV fluidB. Too much of the wrong IV fluidC. The wrong IV fluidD. Hydrochlorthiazide

Question 2

How should she have been treated after 48 h?

A. Water restrictionB. Isotonic salineC. Hypertonic salineD. Hypertonic saline + furosemide

Question 2

How should she have been treated after 48 h?

A. Water restrictionB. Isotonic salineC. Hypertonic salineD. Hypertonic saline + furosemide(Plus urgent nephrology consult)

POSTOPERATIVE HYPONATREMIA: SPECIAL SITUATIONS

Case 2: 43 yr. old g6 p6 woman weighing 116 lb underwent uterine ablation for menorrhagia. Pre-op sodium was 139 mM. Irrigating solution was 3% sorbitol. Eight litres of irrigating fluid was used, effluent volume 4.2 L. In addition, 3.8 L of Ringer's lactate was infused perioperatively. In the recovery room she complained of headache; she had facial puffiness; lethargic, rousable with an unilateral Babinski. Serum sodium was 112 mM, hemoglobin 76 g/L, creatinine 55 uM, urine osmolality 630 mosmol/kg, urine sodium 125 mmol/L 10

Q3

She became hyponatremic because of:

A. Large volume of ringer’s lactateB. Absorption of irrigating solutionC. HemolysisD. ADH release by reduced ECV

Hyponatremia with Hypotonic Irrigating Solutions (eg. TURP, Hysteroscopy) Absorption of electrolyte- free water with

either sorbitol or glycine through vascular bed of prostate or uterus.

Hyponatremia, brain cell swelling Pulmonary edema IVV and se. albumin Encephalopathy from metabolism of

glycine to ammonium.

Incidence 1-4% Prevention: limit duration of procedure, limit

pressure, monitor positive fluid balance

Q3

She became hyponatremic because of:

A. Large volume of ringer’s lactateB. Absorption of irrigating solutionC. HemolysisD. ADH release by reduced ECV

Q3

She became hyponatremic because of:

A. Large volume of ringer’s lactateB. Absorption of irrigating solutionC. HemolysisD. ADH release by reduced ECV

24 year old woman undergoes resection of suprasellar craniopharyngioma. Normal pre-op serum sodium (141). During first hour of surgery passes 700 ml of urine.

Q4

What should you do?A. Give DDAVP and replace urine with

2/3-1/3B. Give DDAVP and replace urine with

isotonic salineC. Replace urine with 2/3-1/3D. Replace urine with isotonic salineE. Do nothing – this will resolve by itself

Pituitary surgeryClassic triphasic pattern initial central DI due to interruption

of hypothalamic-pituitary axis period of SIADH due to leak of ADH

from injured cells chronic central DI

This pattern is uncommon, seen in only 1% of patients

What Actually Happens After Transsphenoidal Pituitary Adenoma Resection – 57 patients

25% no abnormality 40% - diabetes insipidus

Permanent in 10% 20% hyponatremia 15% DI then hyponatremia

J Neurosurg 2009;111:555

Management of Central DI Patients with central DI who are awake

and appreciate thirst do not become hypernatremic – they drink adequate water

An anesthetized patient with central DI is at high risk of acute hypernatremia and brain injury

DDAVP (IV, SC) for acute situations, IN or PO for chronic

Q4

What should you do?A. Give DDAVP and replace urine with

2/3-1/3B. Give DDAVP and replace urine with

isotonic salineC. Replace urine with 2/3-1/3D. Replace urine with isotonic salineE. Do nothing – this will resolve by itself

Q4

What should you do?A. Give DDAVP and replace urine with

2/3-1/3B. Give DDAVP and replace urine with

isotonic salineC. Replace urine with 2/3-1/3D. Replace urine with isotonic salineE. Do nothing – this will resolve by itself

Cerebral Salt Wasting Syndrome

Syndrome of hyponatremia, high ADH, intravascular volume depletion, high urinary sodium loss in association with subarachnoid hemorrhage, trauma, neurosurgical procedures etc.

Pathogenesis unclear; difficult to distinguish from SIADH sometimes

Prevention of Postoperative Hyponatremia

Avoid large volumes of hypotonic fluid unless the patient is hypernatremic

Limit volume of I.V. fluid given to meet patient’s needs

Adjust volume to patient’s body weight

Peri-operative IV Fluid Annals Surgery 2003;238:641 RCT of standard vs restricted IV fluid

in patients undergoing colorectal resection

Multicenter study from Denmark Powered to detect a 20% difference

in complications with 80% power 86 patients per group

Peri-operative IV Fluid -Standard

Intra-op 500 ml HAES 6% in NS Third space loss: NS 7 ml/kg/h X1 h, then

5 ml/kg/h X 2, then .3 ml/kg/h Blood loss: up to 500 ml: 1-1.5 L NS then

HAES Post-op

1-2 L crystalloid/day

Peri-operative IV Fluid Restricted Intra-op:

No preloading No replacement of third space loss Blood loss: volume/volume with HAES

Post-op 1000 ml 5% D/W for remaining OR day Then oral fluid or IV if needed Furosemide if weight increased by 1

kg

Results

Standard

Restricted

IV fluid OR day

5.4 L 2.7 L*

IV fluid POD 1

1.5 L 0.5 L*

Max increase wt

0.9 kg 3.5 kg*

Complications

40 21*

Compl -major 18 8*

Complication frequency related to IV fluid and wt gain on operative day

Meta-analysis of Standard vs Restricted IV Fluid - Colorectal surgery only Restricted fluid strategy reduced

morbidity: OR 0.41 (0.22-0.77) True for pre-operative and intra-

operative restriction but not post-operative)

British J Surg 2009;96:331

ActualPredicte

d

By end of surgery

A Comparison of Albumin and Saline for Fluid Resuscitation in the Intensive Care Unit

NEJM 2004;350:2247 Previous meta-analysis suggested

albumin resuscitation increased mortality

RCT in 7,000 ICU patients 4% albumin vs crystalloid for fluid No difference in mortality

HYPERNATREMIA Water deficiency: may be

excessive water loss (eg sweating, hyperventilation, burns, polyuria) but inadequate intake is always present.

Causes of Poor Intake Coma Conscious but unable to speak or

communicate (intubated in ICU, stroke, infants)

Dementia, elderly (reduced thirst appreciation)

Unable to gain access to water - bedridden elderly

Treatment of Hypernatremia

Replace ongoing losses with similar fluid Restore water deficit with hypotonic

fluid 5% D/W 1/2 normal saline (75 mmol/L) 2/3 - 1/3

Correct chronic hypernatremia slowly: rate of change of serum sodium < 0.5 mmol/L/h

Most Important Messages No hypotonic fluid perioperatively

unless patient is hypernatremic Restrictive fluid therapy seems best

approach for elective abdominal surgery Frequent serum electrolytes following

pituitary/hypothalamic surgery Treat acute symptomatic hyponatremia

urgently with hypertonic saline