Reflective writing 3

In therapy class this week, we went over the case study for diabetes and discussed on how we would
manage a diabetic patient. While discussing the final scenario, we encountered a patient who had
been presenting signs of both hyperosmolar hyperglycaemic state (HHS) and as well as diabetic
ketoacidosis (DKA) . DKA and HHS are to two most severe complication of diabetes. I found it difficult
to differentiate the two conditions and hence, in this essay, I will reflect on what I found out in my
reading on how to clinically differentiate HHS and DKA and how we manage these conditions.

To begin with, HHS and DKA are known as hyperglycaemic crisis. Hyperglycaemic crisis is an
emergency metabolic condition which is associated with uncontrolled diabetes mellitus. Diabetic
ketoacidosis mainly affects patient who have diabetes type 1, which is an absolute insulin dependent
diabetes. This is where there is an insulin deficiency hence lipolysis is not inhibited which results in
the formation of ketone bodies and leads to metabolic acidosis. On the other hand, HHS occur most
commonly in type 2 diabetes, where some amount of insulin is still produced which suppress
lipolysis hence ketones are not formed. In my readings I found out that many of the signs and
symptoms of both of these conditions are similar. For instance, both present with
polyuria, polydipsia, recent weight changes, nausea and vomiting . Also signs of volume
depletion like dry mucous membranes, decreased skin turgor, hypotension,and neurological
abnormalities such as altered mental status, lethargy and coma are also present.

Furthermore, I found out that some signs and symptoms such as abdominal pain, fruity
odour on the breath (from exhaled acetone) and hyperventilation which characteristic of
long, deep breaths (Kussmaul respirations), are more commonly seen in DKA. I also learnt
that usually after the onset of DKA, patient then become aware that they have type1 DM
and become clinically diagnosed with it. HHS, on the other hand, has an insidious onset and
it usually occurs when the type 2 diabetic patient is in stress or sick which gives rise to
counter-regulatory hormones (anti- insulin hormones like cortisol) relative to presently low
insulin levels which causes hyperglycemia and hyprerosmolarity. I also found out that there
are cases where diabetes type 2 patients also get DKA and this is more likely to happen
when the insulin sources has been exhausted.

To add on, in the laboratory testing, the typical outcome for DKA would be hyperglycemia
with high anion gap metabolic acidosis and presences of ketones in the urine. For HHS, the result
would just be hyperosmolarity, hyperglycemia with no ketouria and usually the patient with HHS will
have a higher blood sugar level when compared to DKA.

Moreover, when it comes to the treatment, the criteria is the almost the same for these conditions.
Fluid resuscitation by isotonic fluid is paramount in these patients to correct hypovolemic.
IV insulin is also administered to these patients keeping in mind the serum potassium level
especially for DKA patient. Previously I had not known that insulin therapy is dependent on
the potassium level and how insulin will affect the potassium level if its < 3.3 mEq/l. Since
potassium begins to move back intracellularly after iv insulin, the serum levels will quickly
decrease thus we must make sure that the potassium levels are not low in the first place as
patient will become hypokalemic leading to weakness and decrease heart contractility. So
we look for potassium levels >3.3mEq/l and also prepare for potassium infusion if
<5.3mEq/l. I also read that administration of bicarbonates is controversial as it can worsen
cerebral acidosis.

To conclude, from the readings, I have learnt identify the clinical presentations and other
positives finding in DKA and HSS and the differences between them. I also learnt on the
treatment of this condition. This has also helped me to be aware of the contraindication in
the treatment of hyperglycaemic emergencies