Transcript PRINCIPLES OF SURGERY NOVEMBER 2001 FLUID AND …

PRINCIPLES OF SURGERY
FLUID AND ELECTROLYTE BALANCE
PART 1: DISORDERS OF WATER AND
SALT BALANCE
November 2011
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
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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 fluid
B. Too much of the wrong IV fluid
C. The wrong IV fluid
D. Hydrochlorthiazide
Question 2
How should she have been treated after
48 h?
A. Water restriction
B. Isotonic saline
C. Hypertonic saline
D. Hypertonic saline + furosemide
Water Physiology
Hyponatremia =water excess
Hypernatremia = water deficit
What protects normal humans from hypoor hypernatremia?
PHYSIOLOGY OF ADH AND WATER
Defence against hyponatremia
Q: How would you make someone
hyponatremic?
water
A: Give ___________________
and
ADH
________________________
 ADH (vasopressin) causes collecting duct to
reabsorb water
 HYPONATREMIA = WATER EXCESS (relative
to sodium)
 Usually need water intake and ADH action to
get hyponatremic
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
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ADH is secreted in response to an increasing
serum sodium concentration
Exhibits a threshold and a slope:
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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
ADH vs Serum Sodium:
Threshold and Slope
8
7
6
5
4
3
2
1
0
120
Thirst
125
130
135
140
Serum Na
145
150
155
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 Pathophysiology
How do things go wrong?
HYPONATREMIA
Non-osmotic stimulation of ADH
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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
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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, stress
4. Surgery itself
5. Ectopic secretion by tumours (SCLC)
6. Release from damage to hypothalamus,
posterior pituitary
Why Reduced Effective
Circulating Volume?
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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 increased from 2 uU/ml to 25 uU/ml after
manipulation of viscera during
cholecystectomy; independent of anesthesia
 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
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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
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CAUSE: stimulation of ADH secretion by
surgery (or other factors) + hypotonic
fluid intravenously.
Patients at greatest risk are women,
elderly and children, probably because
they have smaller initial total body water
due to low body weight and higher body
fat
“Postoperative hyponatremia is caused by a
combination of non-osmotic stumuli for ADH
release, such as subclinical volume depletion,
pain, nausea, stress, narcotics etc. and the
administration of hypotonic fluids. It is
estimated that the mortality directly attributable
to hyponatremic encephalopathy in children
with postoperative hyponatremia (sodium <129
mEq/l) is 8%”
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
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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?
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 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 fluid
B. Too much of the wrong IV fluid
C. The wrong IV fluid
D. Hydrochlorthiazide
Question 1
She developed hyponatremia because she
received:
A. Too much IV fluid
B. Too much of the wrong IV fluid
C. The wrong IV fluid
D. Hydrochlorthiazide
Question 2
How should she have been treated after
48 h?
A. Water restriction
B. Isotonic saline
C. Hypertonic saline
D. Hypertonic saline + furosemide
Question 2
How should she have been treated after
48 h?
A. Water restriction
B. Isotonic saline
C. Hypertonic saline
D. 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
10
mmol/L
Q3
She became hyponatremic because of:
A. Large volume of ringer’s lactate
B. Absorption of irrigating solution
C. Hemolysis
D. ADH release by reduced ECV
Hyponatremia with Hypotonic Irrigating
Solutions (eg. TURP, Hysteroscopy)
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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 lactate
B. Absorption of irrigating solution
C. Hemolysis
D. ADH release by reduced ECV
Q3
She became hyponatremic because of:
A. Large volume of ringer’s lactate
B. Absorption of irrigating solution
C. Hemolysis
D. ADH release by reduced ECV
24 year old woman undergoes resection of
suprasellar craniopharyngioma. Normal preop 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 2/31/3
B. Give DDAVP and replace urine with
isotonic saline
C. Replace urine with 2/3-1/3
D. Replace urine with isotonic saline
E. Do nothing – this will resolve by itself
PVN = paraventricular nucleus
SON = supraoptic nucleus
OR – osmoreceptor
br = baroreceptor
Pituitary surgery
Classic 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
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25% no abnormality
40% - diabetes insipidus
• Permanent in 10%
20% hyponatremia
15% DI then hyponatremia
J Neurosurg 2009;111:555
Management of Central DI
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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 2/31/3
B. Give DDAVP and replace urine with
isotonic saline
C. Replace urine with 2/3-1/3
D. Replace urine with isotonic saline
E. Do nothing – this will resolve by itself
Q4
What should you do?
A. Give DDAVP and replace urine with 2/31/3
B. Give DDAVP and replace urine with
isotonic saline
C. Replace urine with 2/3-1/3
D. Replace urine with isotonic saline
E. Do nothing – this will resolve by itself
Cerebral Salt Wasting Syndrome
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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
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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
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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
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Intra-op:
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Post-op
• No preloading
• No replacement of third space loss
• Blood loss: volume/volume with HAES
• 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
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9 RCT’s
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
A Comparison of Albumin and Saline for Fluid
Resuscitation in the Intensive Care Unit
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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
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Water deficiency: may be excessive
water loss (eg sweating, hyperventilation,
burns, polyuria) but inadequate intake is
always present.
Causes of Poor Intake
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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
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Replace ongoing losses with similar fluid
Restore water deficit with hypotonic fluid
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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
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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