Diabetic Ketoacidosis 

CHARACTERISTICS – most commonly seen in type 1 diabetes patients

Pathogenesis –  insulin non compliance, or increased requirements due to increased stress results in lipolysis and ketosis, which leads to the production of beta-hydroxybutyrate and acetoacetate. Both insulin deficiency, and glucagon excess, have a contributory effect to the accelerated hyperglycemia via ketogenesis and lipolysis. INSULIN DEFICIENT, kETONES PRESENT.

KEY FEATURES

Hyperglycemia – due to insulin deficiency 

Positive serum or urine ketones – activation of ketogenesis – testing could give a false negative

Metabolic acidosis – kussmaul respirations compensate for the metabolic acidosis

CLINICAL FEATURES

Nausea or vomiting

kussmaul respirations

Abdominal pain – guarding and rigidity 

Fruity breath

Dehydration, orthostatic hypotension, tachycardia due to volume depletion

polydipsia, polyuria, polyphagia, weakness

Delirium, psychosis, drowsiness, coma may occur

rapid onset of symptoms, usually within 24 hours

DIAGNOSIS

Labs:

Hyperglycemia

Increased anion gap metabolic acidosis

ketonemia and ketouria – acetoacetate is the only ketone body that is picked up by nitroprusside agents – so false negatives may occur 

ketonemia and acidosis are required for diagnosis

Depleted intracellular K levels

OTHER LAB VALUE ABNORMALITIES

Hyperosmolarity

Hyponatremia – will usually resolve itself, caused by shift of fluid from icf to ecf

as insulin is given it will cause a shift of K into skeletal muscle cells and might cause hypokalemia if levels are not high enough before the insulin admin

COMPLICATIONS

Life-threatening mucormycosis – immunocompromised patients

Cerebral edema

Cardiac arrhythmias

TREATMENT

IV insulin

fluid replacement – normal saline.

Replace K prophylactically

if K is below 3.3 hold off on insulin admin until K is 3.3 to 5.2

Give K with fluids to maintain goal of 4 to 5 K

If K is >5.2 do not give any with IVF, but monitor every 2 hours. 

If you give insulin before K levels are restored, it will cause hypokalemia

because there is a severe deficiency of insulin and a contributory presence of glucagon, lipogenesis and ketosis can still be activated.

Lab findings Hyperglycemia >450, Metabolic acidosis(anion gap), ketosis

treatment Insulin, IV fluids, potassium

mortality rate 5-10%

Hyperosmolar Hyperglycemic State(HHS)

Characteristics –  severe hyperglycemia, hyperosmolarity, and dehydration – commonly seen in elderly T2DM patients.

PATHOGENESIS – insulin deficiency – profound hyperglycemia – excessive osmotic diuresis – dehydration and increased serum osmolarity – HHS. Classical presentation in older patients with T2DM and limited ability to drink.  INSULIN PRESENT, KETONES DEFICIENT

In HHS there are low levels of insulin that can lead to hyperglycemia, via gluconeogenesis, but enough will be present to keep lipogenesis and ketogenesis turned off. In HHS patients enough insulin is able to be released to blunt the effect of the counterregulatory hormone, glucagon.  And so just to spell it out ketosis and acidosis are absent or minimal as you might have suspected. 

Key features — Severe hyperosmolarity

CLINICAL FEATURES

thirst, polyuria

hypotension, tachycardia due to dehydration and volume depletion 

seizures may be present

lethargy, confusion, lead to convulsions and coma

DIAGNOSIS

hyperglycemia >900mg/dL

Hyperosmolarity >320mOsm/L

No acidosis

BUN is elevated, azotemia is common

TREATMENT

Fluid replacement – normal saline – 1 L in the first hour – another liter in the next 2 hours – half normal saline once the pt stabilizes.

Glucose levels are lowered as the pt is rehydrated – but the patient will still require insulin – When glucose hits 300mg/dL start 5% glucose.

Rapid lowering of blood glucose might cause cerebral edema in children.  

in patients with cardiac issues or renal disease, avoid overloading these patients.  

Insulin – Make sure K is above 3.3 prior to administration

lab findings. Hyperglycemia >600mg/dL frequently it is >900mg/dL, hyperosmolarity >320, serum pH >7.3 (no acidosis)

So what’s up with the Hypokalemia?

How I am thinking about it is that Insulin, much like catecholamines, will stimulate PKC in muscle cells and stimulate a sodium potassium ATPase. Which pushes Na out of the cell and brings K inside the cell. This sort of makes sense if you think about it in the context of exercise. The ATPase is moving sodium out of the cell in order to get ready for the muscle contractions that require sodium to depolarize the cell and the efflux of K to cause the hyperpolarization. 

This is bad news if the patient has been excreting large amounts of urine and undergoing osmotic diuresis. So the hypokalemia