Question 21

Created on Thu, 05/21/2015 - 16:21
Last updated on Thu, 04/14/2016 - 18:10
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A 77 year old male undergoing transurethral prostatic resection under spinal anaesthesia becomes restless and agitated.  He is intubated and ventilated  in OT, the surgery is expedited, and he is transferred to ICU. His initial biochemistry profile is as follows:


Test

Value

Normal Range

Sodium*

113 mmol/L

135 – 145

Chloride*

87 mmol/L

100 -110

Potassium

4.5 mmol/L

3.2 - 4.5

Glucose

5.1 mmol/L

3.6 – 7.7

Urea

5.0 mmol/L

3.0 – 8.0

Osmolality (measured)

280 mOsm/kg

280 – 300

a)          Describe the important biochemical abnormalities.

b)         What is the likely cause of this confusional state?

c)         What transient neurological disturbance is likely in this clinical setting?

d)         List two confirmatory biochemical features (other than those from the table above).

e)         Do you believe hypertonic saline is indicated? Explain your reasoning.

21.2     Simultaneous arterial blood gas analysis is as follows:

Test

Value

FiO2

0.3

pH

7.33

pO2

93 mm Hg (7.4 kPa)

pCO2

33 mm Hg (4.4 kPa)

HCO3-*

16 mmol/L

Standard base excess*

-9.5 mEq/L

a)  Describe the acid- base status.

b)  What is the mechanism  of this disturbance?

21.3     After 7 hours, the biochemical profile is as follows:

Test

Value

Normal Range

Sodium*

130 mmol/L

135 – 145

Chloride

103 mmol/L

100 -110

Potassium

3.7 mmol/L

3.2 - 4.5

Glucose

5.5 mmol/L

3.6 – 7.7

Urea*

10.6 mmol/L

3.0 – 8.0

Osmolality (measured)

281 mOsm/kg

280 – 300

a)  What important changes have occurred since the initial profile, and how should they be interpreted?

b)  Your registrar is concerned that the sodium is correcting too rapidly. Is there a basis for this concern, and what should be done?

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College Answer

A 77 year old male undergoing transurethral prostatic resection under spinal anaesthesia becomes restless and agitated.  He is intubated and ventilated  in OT, the surgery is expedited, and he is transferred to ICU. His initial biochemistry profile is as follows:


Test

Value

Normal Range

Sodium*

113 mmol/L

135 – 145

Chloride*

87 mmol/L

100 -110

Potassium

4.5 mmol/L

3.2 - 4.5

Glucose

5.1 mmol/L

3.6 – 7.7

Urea

5.0 mmol/L

3.0 – 8.0

Osmolality (measured)

280 mOsm/kg

280 – 300

a)          Describe the important biochemical abnormalities.

Severe normotonic hyponatraemia. The osmolar gap is increased to > 40 mOsm/kg (51 mosm/kg using 1.86*(Na + K) + urea + glucose, or 44 mOsm/kg using 2*Na + urea + glucose).

b)         What is the likely cause of this confusional state?

Absorption of glycine / water irrigation solution causing glycine neurotoxicity. Glycine is an inhibitory neurotransmitter. Increased plasma ammonia may contribute, but the encephalopathy isnot due to a primary increase in brain water.

c)         What transient neurological disturbance is likely in this clinical setting?

Visual impairment, blindness, sometimes fixed pupils. Should completely resolve in a few hours

d)         List two confirmatory biochemical features (other than those from the table above).

Hyperammonaemia, hyperglycinaemia, hyperserinaemia, metabolic acidosis.

e)         Do you believe hypertonic saline is indicated? Explain your reasoning.

None. The osmolality is normal. Hypertonic saline should only be considered if measured osmolality < 260 mOsm/kg (TE Oh p 967)

21.2     Simultaneous arterial blood gas analysis is as follows:

Test

Value

FiO2

0.3

pH

7.33

pO2

93 mm Hg (7.4 kPa)

pCO2

33 mm Hg (4.4 kPa)

HCO3-*

16 mmol/L

Standard base excess*

-9.5 mEq/L

a)  Describe the acid- base status.

Compensated metabolic acidosis – normal anion gap

b)  What is the mechanism  of this disturbance?

Water absorption (SID zero) reducing extracellular SID (in excess of ATOT dilution).

21.3     After 7 hours, the biochemical profile is as follows:

Test

Value

Normal Range

Sodium*

130 mmol/L

135 – 145

Chloride

103 mmol/L

100 -110

Potassium

3.7 mmol/L

3.2 - 4.5

Glucose

5.5 mmol/L

3.6 – 7.7

Urea*

10.6 mmol/L

3.0 – 8.0

Osmolality (measured)

281 mOsm/kg

280 – 300

a)  What important changes have occurred since the initial profile, and how should they be interpreted?

Osmolar gap now greatly reduced (to 16 mOsm/kg, or to 5 mOsm/kg using simple formula), indicating rapid glycine elimination. Sodium rapidly normalising, but plasma still normotonic

b)  Your registrar is concerned that the sodium is correcting too rapidly. Is there a basis for this concern, and what should be done?

Rapid sodium correction is to be expected during glycine elimination, and is safe provided no sudden changes in osmolality.

Discussion

The story given by the college makes one think immediately of the TURP syndrome, a cause of isoosmolar hyponatremia, which is seen less frequently these days because of a shift away from glycine-containing irrigation solutions.

a) The first part of the question asks about the important biochemical abnormalities. The college answer describes it as "normotonic hyponatremia". This is accurate, given that the given osmolality lies within the normal range of tonicity.

The osmolar gap is raised:

280 - (113 × 2 + 5.1 + 5) = 43.9

And so, this confirms one's instant impression that this a glycine-associated hyponatremia is causing this confusional state.

b) What is the likely cause of this confusional state?

Of the offered biochemistry values, only hyponatremia stands out.

However, it is not alone in the pathogenesis of this confusion.

Glycine itself has a well-known toxicity syndrome, and on top of that its metabolism by oxidative deamination can result in a massive excess of ammonia, with its own delirium-generating effects.

c)What transient neurological disturbance is likely in this clinical setting?

Traditionally, glycine toxicity causes blindness. Stupour and coma are also common. A good article on this topic has a table (Table 1) which lists other unpleasant CNS manifestations, including dilated unreactive pupils, seziures and paralysis.

d)List two confirmatory biochemical features (other than those from the table above).

Glycine toxicity is associated with the following biochemical changes, of which some have already been identified by the abovementioned test panel.

  • Hyponatremia
  • Hypoosmolarity
  • Hyperglycinaemia
  • Hyperammonaemia
  • Hyperserinaemia
  • Hyperoxalaemia
  • Metabolic acidosis: NAGMA due to absorption of fluid with a low strong ion difference, and HAGMA due to excess of oxalate and serine.

e) Hypertonic saline is not indicated in this setting; the serum sodium will return to normal when the glycine and free water have been eliminated, which does not take long. The neurological features of this syndrome are not due to cerebral oedema, but rather due to the direct neurotoxicity of the glycine, and thus one cannot call this "symptomatic hyponatremia".

21.2: The college asks us to interpret the ABG.

Let us do it systematically.

  1. The A-a gradient is high:
    PAO2 = (0.3 × 713) - (33 × 1.25) = 172.65
    Thus, A-a = ( 172.65 - 93) = 79.65mmHg.
  2. There is acidaemia
  3. The PaCO2 is compensatory
  4. The SBE is -9.5, suggesting a metabolic acidosis
  5. The respiratory compensation is adequate:
    the expected PaCO2 is (16 × 1.5) + 8 = 32mmHg
  6. The anion gap is slightly raised, but almost normal:
    (113+4.5) - (87+16) = 14.5
    The delta ratio suggests that there is a combined normal anion gap and high anion gap metabolic acidosis here.
    (14.5 - 12) / (24-16) = 0.31

This is a consequence of absorbing pure water (which has an SID of 0) as well as a minor contribution from oxalate and serine.

21.3

a)  What important changes have occurred since the initial profile, and how should they be interpreted?

The college now presents us with an essentially normal biochemical profile. The osmolar gap is now normal:

281 - (130 × 2 + 5.5 + 10.6) = 4.9

The glycine has therefore been eliminated.

b)  Your registrar is concerned that the sodium is correcting too rapidly. Is there a basis for this concern, and what should be done?

The panicky registrar needs to be calmly reassured. The elimination of glycine has resulted in the normalisation of sodium, which is as rapid in onset as the hyponatremia. Only chronic hyponatremia needs to be worried about. Because the serum osmolality remains essentially unchanged, there is no danger of cerebral oedema.

 

References

Rhymer JC, Bell TJ, Perry KC, Ward JP. Hyponatraemia following transurethral resection of the prostate. Br J Urol. 1985 Aug;57(4):450-2.

Hahn, R. G. "Serum amino acid patterns and toxicity symptoms following the absorption of irrigant containing glycine in transurethral prostatic surgery." Acta anaesthesiologica scandinavica 32.6 (1988): 493-501.

Roesch, Ryland P., et al. "Ammonia toxicity resulting from glycine absorption during a transurethral resection of the prostate." Anesthesiology 58.6 (1983): 577-578.

Glycine Toxicity page from The Anesthesia Practice Manual for Spectrum by Tom VerLee.

Gravenstein, Dietrich. "Transurethral resection of the prostate (TURP) syndrome: a review of the pathophysiology and management." Anesthesia & Analgesia 84.2 (1997): 438-446.

Hahn, R. G., and M. Rundgren. "Vasopressin and amino acid concentrations in serum following absorption of irrigating fluid containing glycine and ethanol."British journal of anaesthesia 63.3 (1989): 337-339.

Stewart, PA Hamilton, and I. M. Barlow. "Metabolic effects of prostatectomy."Journal of the Royal Society of Medicine 82.12 (1989): 725-728.

Beal, J. L., et al. "Consequences of fluid absorption during transurethral resection of the prostate using distilled water or glycine 1.5 per cent." Canadian Journal of Anaesthesia 36.3 (1989): 278-282.

Fitzpatrick, J. M., G. P. Kasidas, and G. Alan Rose. "Hyperoxaluria following glycine irrigation for transurethral prostatectomy." British journal of urology 53.3 (1981): 250-252.