Question 10

College Answer

Candidates were expected to outline each of the important abnormalities and how they should influence her management. One approach would be the following:

•    The biochemistry supports a diagnosis of hyperosmolar hyperglycaemic syndrome, with post-ictal lactic acidosis. There is also a likely component of ketoacidosis.

•    The high urea / creatinine ratio confirms significant dehydration – most people with this condition are at least 10% dehydrated by body weight – usually more. She will require steady rehydration over 12 to 24 hours.

•    The sodium adjusted to normoglycaemia is about 153 mmol/L. This means that, after intravascular volume is restored with isotonic fluids, rehydration should be conducted with relatively hypotonic fluids eg 0.45% saline initially.

•    The metabolic acidosis is uncompensated. The minute ventilation should be increased (if this can be done safely), to replicate appropriate respiratory compensation.

•    There is a raised anion gap (34.5 mEq/L without K). The degree of lactate elevation is insufficient to explain the anion gap, indicating probable co-existing ketoacidosis. Beta- hydroxybutyrate should therefore be measured. An insulin infusion (0.1 U/kg/hr) is required for gentle glucose correction and reversal of ketoacidosis.

•    The plasma potassium is already reduced, indicating a severe deficit and the need for immediate replacement in the absence of anuria. She is likely to need 10 - 20 mmol/hr or more for many hours, since the total deficit will exceed 6 mmol/kg.

•    Blood gases, Na, K and glucose will need frequent (hourly) measurement initially. Rapid reductions in osmolality should be avoided (using sodium adjusted to normoglycaemia as a surrogate).

The A-a gradient is significantly elevated at 380 mm Hg. This could indicate aspiration pneumonitis, pneumonia, or segmental collapse – even endobronchial intubation. These possibilities should be looked for clinically and on CXR.

Discussion

Let us dissect these results systematically.

1. The A-a gradient is high:
   PAO₂ = (713) - (43 × 1.25) = 659.25
   Thus, A-a = ( 659.25 - 280) = 379.25mmHg.
2. There is acidaemia
3. The PaCO₂ is not compensatory
4. The SBE is -16.8, suggesting a severe metabolic acidosis
5. The respiratory compensation is inadequate - the expected PaCO₂(11.5 × 1.5) + 8 = 25.25mmHg, and thus there is also a respiratory acidosis
6. The anion gap is (128) - (82 + 11.5) = 34.5, or 37.6 when calculated with potassium.
   The delta ratio, assuming a normal anion gap is 12 and a normal bicarbonate is 24, would therefore be (34.5 - 12) / (24 - 11.5) = 1.8. 
   This delta ratio suggests that there is a pure high anion gap metabolic acidosis here, with perhaps just a hint of pre-existing metabolic alkalosis.
    

The lactate is 9.2, which does not account for much of the anion gap, suggesting that other unmeasured anions are present.

If one were to ignore the HONK, one would leave it at that.

However, most people would notice that the glucose is 79.

This is slightly abnormal. And it influences the sodium value.

The corrected sodium is 128 + (glucose/4), or 147.8 mmol/L.

Because the college do not show their working, it is impossible to say how they managed to get a sodium value of 153. If one were to use the standard formula, one gets 147.75mmol/L.

One may also use a slightly less standard formula, where for every 5.6mmol/L of glucose, the sodium decreases by 1.6mmol/L for the first 25mmol of glucose, and by 2.4mmol/L for hyperglycaemia above 25mmol/L. In such a case, the corrected sodium is 158:

= measured Na⁺ plus (25 / 5.6) × 1.6, plus [(79-25)/5.6]× 2.4

In any case, there is hypernatremia.

Anyway. The college question asks how any of this information would influence your management.

I will go through the abnormalities systematically.

• Acidosis
  • This is a combination of several contributing aetiologies:
    • uremic acidosis
    • post-ictal lactic acidosis
    • ketoacidosis
    • respiratory acidosis
  • The ketoacidosis should be confirmed with a blood ketone (hydroxybutyrate) level.
  • Management would consist of the following meaasures:
    • careful rehydration
    • insulin therapy (the college recommends 0.1 unit/kg/hr)
    • increased minute ventilation
• Hypokalemia
  • According to HONK literature, the total deficit will likely exceed 5-15mmol/kg. Aggressive replacement is in order.
• A-a gradient
  • For whatever reason, this patient is relatively hypoxic.
  • This should be investigated clinically, and with a CXR.

Hyperglycemic Comas by P. VERNON VAN HEERDEN from Vincent, Jean-Louis, et al. Textbook of Critical Care: Expert Consult Premium. Elsevier Health Sciences, 2011.

 

Oh's Intensive Care manual: Chapter 58  (pp. 629) Diabetic  emergencies  by Richard  Keays

 

Umpierrez, Guillermo E., Mary Beth Murphy, and Abbas E. Kitabchi. "Diabetic ketoacidosis and hyperglycemic hyperosmolar syndrome." Diabetes Spectrum15.1 (2002): 28-36.

 

ARIEFF, ALLEN I., and HUGH J. CARROLL. "Nonketotic hyperosmolar coma with hyperglycemia: clinical features, pathophysiology, renal function, acid-base balance, plasma-cerebrospinal fluid equilibria and the effects of theraphy in 37 cases." Medicine 51.2 (1972): 73-94.

 

Gerich, John E., Malcolm M. Martin, and Lillian Recant. "Clinical and metabolic characteristics of hyperosmolar nonketotic coma." Diabetes 20.4 (1971): 228-238.

 

Kitabchi, Abbas E., et al. "Hyperglycemic crises in adult patients with diabetes." Diabetes care 32.7 (2009): 1335-1343.

 

Kitabchi, Abbas E., et al. "Hyperglycemic crises in adult patients with diabetes a consensus statement from the American Diabetes Association." Diabetes care 29.12 (2006): 2739-2748.

 

Ellis, E. N. "Concepts of fluid therapy in diabetic ketoacidosis and hyperosmolar hyperglycemic nonketotic coma." Pediatric clinics of North America 37.2 (1990): 313-321.

 

Pinies, J. A., et al. "Course and prognosis of 132 patients with diabetic non ketotic hyperosmolar state." Diabete & metabolisme 20.1 (1993): 43-48.