Epidemiology

Over 100,000 cases of DKA, 5000 cases of diabetic

coma, and 10,000 cases of hyperosmolar coma were
recorded in the United States between 1989 and
1991
DKA is the most common cause of diabetes-related
death in childhood and adults
1/5 to 1/3 of patients with classic DKA will also have
hyperosmolarity
About to of patients with uncontrolled diabetes
will have an osmolarity of 320 mOsm or more
diabetic emergencies has remained unchanged for
the past 10 years.
 Pathophysiology
Low blood glucose triggers the release of glucagon
from pancreatic alpha cells (stimulates the release
of glucose, breakdown of fat and protein) resulting
weight loss
High blood glucose triggers the release of insulin
from pancreatic beta cells
Glucocorticoids, ACTH and growth hormone released
from the pituitary, increase blood glucose levels by
inhibition of glucose uptake by tissues
epinephrine, stimulates the production of glucose by
activation of glycogenolysis in response to stress
 glucagon, cortisol,catecholamines, and growth
hormones) are increased because the cells cant use
the available glucose
Increased hepatic glucose production and decreased
peripheral uptake of glucose
lack of insulin and excess of glucagon, so the excess
glucose accumulates in the bloodstream
Breakdown of fat produce fatty acid oxidation leads to
ketone body formation leads to acidosis
Blood glucose levels will rise above the renal
threshold or glucose reabsorption resulting osmotic
diuresis causing in significant volume depletion
 DKA
DKA is characterized by
hyperglycemia with glucose over 250 mg/dL (12.5)
marked ketoacidosis, pH levels less than 7.35, low serum bicarbonate (under 15
mmol/L)
Positive urine ketone
A high anion gap
Typical signs include fatigue, malaise, thirst, polyuria, reduced, skin
elasticity (poor skin turgor), dry mucous membranes, hypotension, and
tachycardia from the volume deficits
note weight loss if there is a long onset
The exact cause of the abdominal pain associated with DKA is not known
If the patient is carefully examined, the rapid, deep breathing typical of
Kussmaul respirations is often found
Coma may result from the hyperosmolality associated with DKA.
A calculated osmolality greater than 320 mOsm/L is often associated with
coma
 The differential diagnosis in diabetes and findings of DKA
includes:
HHS
Alcoholic ketoacidosis
Starvation
Sepsis
Lactic acidosis
Uremia
Starvation ketosis and alcoholic ketoacidosis excluded
clinical history
plasma glucose mildly elevated (rarely 250 mg/dL) to hypoglycemia
Alcoholic ketoacidosis can result in profound acidosis
in starvation ketosis is usually serum bicarbonate concentration less
pronounced than in DKA.
 HHS
HHS is characterized by a marked hyperglycemia (plasma
glucose is more than 600 mg/dL (30) with serum
osmolarity greater than 350 mOsm, dehydration, and lack
of insulin
Mean age of onset in the seventh decade of life
Males are affected slightly less often than females
mortality rates as high as 12%-46% have been recorded
Wachtel et al found an increasing mortality associated
with increasing age10% among those less than 75
years, 19% in those 75-84 years old, and 35% among
those older than 85 years
Most deaths caused by HHS occur within the first 1-2
days.
 Initial features of HHS include fatigue, blurred vision,
polydipsia, muscle cramps, and weight loss
may also complain of muscle cramps, nausea,
vomiting, or abdominal pain
typical patient is elderly, volume depleted, and
comatose or with an altered mental status
Patients with HHS often present with neurologic
abnormalities
Seizures are seen in up to 25% of patients, transient
hemiparesis, movement disorders or like a stroke
coma should not be attributed to hyperosmolality
when the osmolality is less than 320 mOsm/kg.
 Hyperglycemia
Polyuria
Polydipsia
Polyphagia
Weight loss
Fatigue and weakness
Abdominal pain
may be due to pancreatitis or
disease that precipitated the DKA.
DKA is often mistaken for gastroenteritis.
Nausea and vomiting
Acidosis Cerebral Edema
Hyperventilation Decreasing sensoria
This is due to the Sudden and severe headache
metabolic acidosis. Change in vital signs
(hypothermia, hypotension,
Acidosis may be hypertension, tachycardia,
mistaken for bradycardia, gasping
hyperventilation respirations, periods of
apnea)
syndrome. Ophthalmoplegia
Altered mental status, Pupillary changes
this can vary from Papilledema
lethargy to coma. Posturing, seizures
 Important point in history
1. Are any symptoms consistent with
hyperglycemia, acidosis, or cerebral edema
present
2. Does the patient have diabetes? If so, has
the patient had prior episodes of DKA or HHS?
20%-30% of cases of DKA is initial presentation of
previously undiagnosed diabetes, symptoms are gradual
in onset with progressive dehydration and slowly
developing ketosis
In DM patient, DKA develop rapidly, occur during an
illness or defaulted OHA or insulin therapy. Ketoacidosis
may predominate, and DKA may present with only a
modest elevation of the blood glucose (250 mg/dL).
 3. Is there an associated
infection?
must search diligently in these patients
for a focus of infection such as sinusitis,
middle ear infections, prostatitis,
perirectal abscess, pneumonia, urinary
tract infection
Rectal and pelvic examinations are
important
 4. Is there another associated illness?
Cerebrovascular accidents (both stroke and intracranial
hemorrhage)
Myocardial infarction
Acute pancreatitis
Pulmonary embolus
Mesenteric thrombosis
Renal failure
Heat stroke and heat stress
Gastrointestinal hemorrhage
Hypothermia
Alcohol consumption or cocaine use
 5. Has the patient been receiving adequate
insulin?
Failure to take insulin is the most common cause of
recurrent DKA
6. What other medications has the patient
been taking?
sympathomimetics, pentamidine, thiazides, phenytoin,
and calcium-channel blocker agents can precipitate
diabetes and DKA
Drug induced hyperglycemia may precipitate HHS,
include azathioprine, beta-blocking agents, cimetidine,
diuretics, glycerol, phenothiazines, calcium-channel
blocking agents phenytoin, and steroids
 The anion gap:
Na+ -(Cl- + HCO3-)
Correction of serum sodium:
Na+ + 1.6 * [(glucose in mg/dL) 100] / 100
Calculation of effective serum
osmolality:
2[Na+ + K+ ] + [glucose in mg/dL]/18
Total body water deficit:
0.6 x weight x [1-140/serum sodium]
 DKA
Fluid
The most important intervention in DKA
If hypotensive, 1 to 2 litre NS bolus over 1 hour,
may repeat if remain hypotensive
If normotensive, run 1 litre NS over 1 hour
Fluid therapy may complicate pulmonary edema,
may need to auscultate lung, monitor urine
output, in pt with CCF and ESRF may need CVP
In general fluid therapy 4 to 14 ml/kg/hour
Aim to replace deficit over 8 hours, another
over 16 hours
 Insulin
Insulin aim to treat ketosis, acidosis, hyperglycemia
Infusion vs IM
Smaller dose for good eficacy
Smooth correction, flexible to adjust
Start 0.1u/kg/hr
s/c insulin not recommended due to poor
absorption
Bolus vs infusion
Boluses causing rapid reduction of potassium
Lethal complication
 Bicarbonates
Not recommended
Mask the ketoacidosis
Increased risk of cerebral edema
American Diabetics Association recommended if ph less
than 6.9
Potassium
Administration of insulin, resolution of acidosis will causing
massive shift of extracellular potassium into the cell
Insulin therapy should not be start till K level is known
Only start the fluid resust
One level K less than 5, ECG show no tall T, and good urine
output, may start K
 Phosphate
not shown any clear benefit to phosphate
replacement in DKA
Indications for the clinical repletion of phosphate
include left ventricular dysfunction or failure to
clear mental confusion despite improvement in
circulating volume, hyperosmolarity, and acidosis
phosphate level is less than 1.0 mg/dL or if one of
the above indications for phosphate therapy is
present, then give 30-60 mM of phosphate over a
24-hour period.
 Magnesium
Significant magnesium depletion usually
is associated with hypocalcemia and
hypokalemia
Severe hypomagnesemia can lead to
both atrial and ventricular arrhythmias
level of less than 1.8 mEq/L or has tetany,
then magnesium sulfate may be started
as 5 grams in 500 mL of normal saline
administered over five hours
 Cerebral edema
It is almost always a disease of children;
over 95% of cases in the largest reported series occurred
under the age of 20, and one-third of cases occurred under
the age of 5 years
One-fourth of the children affected, die from this complication
The patient develops increasing irritability, central nervous
system depression, seizures, and coma (Cerebral edema
complicating DKA)
Bicarbonate is associated with several risks, including cerebral
edema, and should be avoided if possible.
use of mannitol as an osmotic diuretic to lower the intracranial
pressure. Recent studies show that for maximum effect,
mannitol should be given within 5-10 minutes of the initial
deterioration in neurologic function.