A 56 year old, homeless man was admitted to the Emergency Department with clinical features suggestive of a bowel obstruction.  As he is confused, it is not possible to elicit a clear history.

The first set of blood tests show:

Test

Value

Normal Range

Sodium

137 mmol/L

(137 – 145)

Potassium

4.0 mmol/L

(3.1 – 4.2)

Chloride*

98 mmol/L

(101 – 109)

Bicarbonate*

15 mmol/L

(22 – 32)

Glucose*

48 mmol/L

(4.0 – 6.0)

Urea*

18 mmol/L

(3.0 – 8.0)

Creatinine*

0.2 mmol/L

(0.05 – 0.12)

a)  Outline the possible causes of his metabolic acidosis.

b)  What is the corrected serum sodium?

c)  Outline your approach to the correction of his metabolic abnormalities.

d) List the possible complications of this condition and its treatment.

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College Answer

a)  Outline the possible causes of his metabolic acidosis.

High anion gap metabolic acidosis

Lactic acidosis 
•    Severe dehydration from osmotic diuresis from hyperglycaemia.
•    Ischaemic bowel
•     Sepsis
•    Metformin (if known type 2 diabetes)

Keto-acidosis 
•  Diabetic (unlikely to be first presentation at 56 yrs with type I diabetes)
•  Alcoholic keto-acidosis (possible although sugar too high)
•  Starvation keto-acidosis (possible although sugar too high)

Toxins

Salicyates, methanol, ethylene glycol,

Renal Failure

b)  What is the corrected serum sodium?

Corrected Sodium= Measured sodium + glucose/4 (Credit was given to people using a range of different formulae) approximately =149 mmol/L.

c)  Outline your approach to the correction of his metabolic abnormalities.

Fluid replacement:
Generally Normal Saline/Hartmanns solution, even if hypernatraemia present to expand ECF volume rapidly.

After initial restoration of normotension, free water replacement .
Fluid titrated to clinical status- organ perfusion, filling pressures, etc. Elderly patients with likely co-existent cardiac disease need more careful monitoring/less aggressive replacement

•     Insulin
-       Blood glucose can fall rapidly when urine output re-established and dehydration corrected. High risk of hypoglycaemia.
-      Treatment with insulin to decrease the serum osmolality by no greater than
2mosmol/kg/hr and blood glucose by no more than 3-4mmol/hr

•     Electrolytes potassium supplements required. Attention to magnesium and phosphate supplementation also required.

•     Correction of underlying cause (in this case, surgery for bowel obstruction)

d)             List the possible complications of this condition and its treatment.

• Cerebral oedema with rapid correction
• Pre-renal azotaemia & renal failure
•  Shock 
• Hypercoagulable state-  thromboembolic complications- DVT, stroke, AMI
• Fluid overload/congestive  cardiac failure with correction
• Metabolic and electrolyte abnormalities- hypokalaemia,
• hypomagnesaemia,  hypophosphataemia,  hypoglycaemia, hyperchloraemic
(non-anion gap) acidosis (normal saline therapy)
• Infections and sepsis

Discussion

In this question, the candidates are presented with a picture closely resembling a HONK.

The proper calculation of the anion gap is fuddled by the presence of vast quantities of glucose, and thus an inaccurate reported sodium.

Unadjusted, the biochemistry suggests that the anion gap may be significantly raised:

(137 + 4) - (98 + 15) = 28.

However, if we adjust the sodium, we find that it is even worse.

(149 + 4) - (98 + 15) = 40

Thus, the candidate ought to remember that up-adjusting the sodium for hyperosmolar states will only make the anion gap wider.

The delta ratio, calculated from the corrected and uncorrected anion gaps, is either 1.7 or 3.1

(28 - 12) / ( 24 - 15) or (40 - 12) / (24 - 15)

Thus, there is a high anion gap metabolic acidosis which coexists with a metabolic alkalosis.

a) Outline the possible causes of his metabolic acidosis.

The list of differentials provided by the college is comprehensive.

One may divide it into a MUDPILES mnemonic, or organise it by unmeasured anions:

  • Lactate:
    • Hypovolemic shock
    • Sepsis
    • Cardiogenic shock
    • Mitochondial toxicity
    • Thiamine deficiency
    • Biguanide poisoning
  • Toxic metabolites
    • Methanol
    • Ethylene glycol
  • Ketoacids
    • Diabetic ketoacidosis
    • Alcoholic ketoacidosis
    • Starvation ketoacidosis
  • Unmeasured non-volatile metabolic acids
    • Renal failure

b) What is the corrected serum sodium?

The college gave the candidates credit for mentioning a number of formulae.

There are indeed several different ways of calculating the corrected sodium.

They all follow the same trend: Corrected Na+ = measured Na+ + (correction factor)

The correction factor is a matter of debate, and there are several variations:

  • Glucose in mmol/L divided by 4
  • (Glucose in mg/dL - 100) multiplied by 0.016
  • (Glucose in mg/dL - 100) multiplied by 0.024

c) Outline your approach to the correction of his metabolic abnormalities.

One would not need to approach this in an algorithmic fashion. It is a question specifically about the metabolic abnormalities, and so one does not need to go on at lengths about securing the airway.

Thus:

  • Correct fluid deficit with fluid resuscitation
  • Correct hyperglycaemia with insulin
    • careful monitioring for hypoglycaemia (the college points out that once the renal function begins to recover, urinary losses of glucose will be rapid)
  • Correct electrolytes by careful monitoring and replacement
  • Correct underlying disorder (bowel obstruction)

d) List the possible complications of this condition and its treatment.

Complications of HONK are discussed in greater detail elsewhere.

In brief, the major ones are listed below:

  • Cardiac arrest
  • Cardiovascular collapse
  • Myocardial infarction
  • Stroke
  • Cerebral oedema and brain injury
  • Venous thrombosis

In addition to these, the college has thrown in infection/sepsis as a complication of bowel obstruction, as well as complication of HONK management (electrolyte bewilderment and fluid overload).

References

References

Hillier, Teresa A., Robert D. Abbott, and Eugene J. Barrett. "Hyponatremia: evaluating the correction factor for hyperglycemia." The American journal of medicine 106.4 (1999): 399-403.

Roscoe, J. M., et al. "Hyperglycemia-induced hyponatremia: metabolic considerations in calculation of serum sodium depression." Canadian Medical Association Journal 112.4 (1975): 452.