This case report describes a 25-year-old man with a history of type 2 diabetes who presented with diabetic ketoacidosis (DKA). He reported symptoms of nausea, vomiting, polyuria, polydipsia and weight loss. Laboratory results showed metabolic acidosis, hyperglycemia and ketones consistent with DKA. While being treated for DKA, he developed worsening back pain and new neurological symptoms. Imaging revealed an epidural abscess, which was surgically treated. He required intensive rehabilitation for residual lower extremity weakness following treatment and resolution of the abscess.

1. 1. Diabetic Ketoacidosis (DKA)
2. Hyperosmolar Hyperglycemic State (HHS)
3. Hypoglycemia

2. Case Presentation
 R.T., a 25-year-old African-American man with
type 2 diabetes presented with a 5-day history of
nausea and vomiting. He also reported a 2-week
history of polyuria and polydipsia and a 10-lb
weight loss. A review of symptoms was pertinent
for a 5-day history of persistent lower back pain.
The patient was diagnosed with type 2 diabetes 5
years ago when he presented to a different
hospital with symptoms of polyuria, polydipsia,
and weight loss. He was given a prescription for a
sulfonylurea, which he says he took until his initial
prescription ran out 1 month later. He had not
taken any other medication since that time.

3. Case Presentation
 Physical examination revealed an afebrile, obese man
(BMI 40 kg/m2) with prominent acanthosis nigricans,
no retinopathy by direct funduscopic exam, and a
normal neurological exam, including motor function
and sensation. The patient had no tenderness to
palpation over the lumbrosacral spine or paraspinous
muscles despite his complaint of lower back pain. The
laboratory data showed an anion gap, metabolic
acidosis, and hyperglycemia (pH of 7.14, anion gap of
24, bicarbonate 6 mmol/l, urinary ketones 150 mg/dl,
glucose 314 mg/dl) consistent with the diagnosis of
DKA. His white blood count was 20,400/l. Urinalysis
demonstrated no evidence of infection. The patient’s
hemoglobin A1c (A1C) was 13.5%.

4. Case Presentation
 The patient was admitted and treated aggressively
with intravenous fluid and an insulin-glucose
infusion.
 A non-contrast magnetic resonance imaging (MRI)
of the lumbosacral spine (L-spine) was obtained
because of the patient’s persistent complaint of
lower back pain. The Lspine MRI results were
negative for pathology. However, R.T. reported
increasing discomfort and now noted weakness
and numbness in his bilateral lower extremities.

5. Case Presentation
 Neurology was consulted, and during their
assessment, the patient became incontinent and
was found to have 0/5 strength in the lower
extremities, severely compromised sensation, and
decreased rectal tone. A contrast MRI of both the
thoracic and lumbar spine was ordered, and the
patient was found to have a T10–T12 epidural
abscess. The patient’s antibiotic coverage was
broadly expanded, high-dose intravenous steroids
were initiated, and neurosurgery was urgently
consulted. Emergent evacuation of the epidural
abscess with laminectomies of T10–T12 was
performed without complication.

6. Case Presentation
 R.T.’s neurogenic bladder resolved
without further intervention. After
intensive inpatient rehabilitation, he had
3/5 strength in bilateral lower extremities
and was still unable to ambulate.

7. DKA
HHSMild Moderate Severe
Plasma glucose
(mg/dL)
> 250 > 250 > 250 > 600
Arterial pH 7.25 – 7.30 7.00 – 7.24 < 7.00 > 7.30
Bicarbonate
(mEq/L)
15 - 18 10 - 14 < 10 > 18
Urine ketones (+) (+) (+) Small
Serum ketones (+) (+) (+) Small
Serum Osmolality
(mOsm/kg)
Variable Variable Variable > 320
Anion Gap > 10 > 12 > 12 Variable
Consciousness Alert Alert/drowsy Stupor/Coma Stupor/Coma

8. Formula
 Serum osmolality
2[measured Na (mEq/L)] + glucose (mg/dL)/18.
 Anion gap
(Na+) - (Cl- + HCO3-) (mEq/L)

9. Precipitating Factors
 Infection (pneumonia, UTI)
 Inadequate insulin therapy
 Acute myocardial infarction, stroke,
pancreatitis
 New onset DM type 1 (especially DKA)

10. Anamnesis
 Symptoms of marked hyperglycemia:
polyuria, polydipsia, and weight loss
 Neurologic symptoms: lethargy, coma
 Hyperventilation and abdominal pain:
limited to patients with DKA

11. Pathophysiology
 Hyperosmolarity  neurologic
symptoms (more frequent in HHS
because greater degree of
hyperosmolarity in HHS than DKA 
hemiparesis or hemianopsia, and/or
seizures
 Severe acidosis in DKA  neurologic
symptoms

12. Pathophysiology
 Osmotic diuresis: glucose osmotic diuresis 
water loss in excess of sodium and potassium 
hyperosmolar state
 The presence of stupor or coma in diabetic
patients with an effective plasma osmolality lower
than 320 mosmol/kg demands immediate
consideration of other causes of the mental status
change.

13. Pathophysiology
 Abdominal pain in DKA: has never been found in
HHS

14. Absolute Insulin
Deficiency
LYPOLYSIS
FFA to liver
KETOGENESIS
KETOACIDOSIS
COUNTER-REGULATORY
HORMONES
Relative Insulin
Deficiency
Absent or minimal
ketogenesis
Proteolysis Proteogenesis
Gluconeogenic
substrates
Glucose
utilization
Glycogenolysis
HYPERGLYCEMIA
Osmotic diuresis
Loss of water & K,
Na retention
DEHYDRATION
Hypovolemia-induced
Hyperaldosteronism
HYPOKALEMIA

15. Clinical features of DKA
 DKA usually evolves rapidly over a 24-hour period.
 Common, early signs of ketoacidosis include
nausea, vomiting, abdominal pain, and
hyperventilation.
 The earliest symptoms of marked hyperglycemia
are polyuria, polydipsia, and weight loss. As
hyperglycemia worsens, neurologic symptoms
appear, and may progress to include lethargy,
focal deficits, obtundation, seizure, and coma.
 Common causes of DKA include: infection;
noncompliance, inappropriate adjustment, or
cessation of insulin; new onset diabetes mellitus;
and myocardial ischemia.

16. Evaluation and laboratory findings of
DKA
 Assess vital signs, cardiorespiratory status, and
mental status.
 Assess volume status: vital signs, skin turgor,
mucosa, urine output.
 Obtain the following studies: serum glucose,
urinalysis and urine ketones, serum electrolytes,
BUN and creatinine, plasma osmolality, arterial
blood gas, venous blood gas, electrocardiogram;
add serum ketones if urine ketones present.
 Additional testing is obtained based on clinical
circumstances and may include: blood or urine
cultures, lipase, chest x-ray.

17. Evaluation and laboratory findings of
DKA
 Diabetic ketoacidosis (DKA) is characterized by
hyperglycemia, an elevated anion gap metabolic
acidosis, and ketonemia. Dehydration and
potassium deficits are often severe.
 Serum glucose is usually greater than 250 mg/dL
(13.9 mmol/L) and less than 800 mg/dL (44.4
mmol/L). In certain instances (eg, insulin given
prior to ED arrival), the glucose may be only mildly
elevated.

18. Management of DKA: Replete fluid deficits
 Give several liters of isotonic (0.9 percent) saline as
rapidly as possible to patients with signs of shock.
 Give isotonic saline at 15 to 20 mL/kg per hour, in the
absence of cardiac compromise, for the first few hours
to hypovolemic patients without shock.
 After intravascular volume is restored, give one-half
isotonic (0.45 percent) saline at 4 to 14 mL/kg per hour
if the corrected serum sodium is normal or elevated;
isotonic saline is continued if the corrected serum
sodium is reduced.
 Add dextrose to the saline solution when the serum
glucose reaches 200 mg/dL (11.1 mmol/L).

19. Management of DKA: Replete K+ deficits
 Regardless of the initial measured serum potassium,
patients with DKA have a large total body potassium
deficit.
 If initial serum K+ is below 3.3 mEq/L, hold insulin and
give K+ 20 to 30 mEq/hour IV until K+ concentration is
above 3.3 mEq/L.
 If initial serum K+ is between 3.3 and 5.3 mEq/L, give
K+ 20 to 30 mEq per liter IV fluid; maintain K+ between
4 to 5 mEq/L.
 If initial serum K+ is above 5.3 mEq/L do not give K+;
check K+ every 2 hours.

20. Management of DKA: Give insulin
 Do not give insulin if initial serum K+ is below 3.3
mEq/L; replete K+ first.
 Give all patients without a serum K+ below 3.3 mEq/L
regular insulin. Either of two regimens can be used: 0.1
units/kg IV bolus, then start a continuous IV infusion 0.1
units/kg per hour; OR do not give bolus and start a
continuous IV infusion at a rate of 0.14 units/kg per
hour.
 Continue insulin infusion until ketoacidosis is resolved,
serum glucose is below 200 mg/dL (11.1 mmol/L), and
subcutaneous insulin is begun.

21. Management of DKA:
Give sodium bicarbonate to patients with pH
below 7.00
 If the arterial pH is between 6.90 and 7.00, give 50 meq
of sodium bicarbonate plus 10 meq of potassium
chloride in 200 mL of sterile water over two hours.
 If the arterial pH is below 6.90, give 100 meq of sodium
bicarbonate plus 20 meq of potassium chloride in 400
mL sterile water over two hours.

23. HHS Guideline

24. HYPOGLYCEMIA
 Blood glucose < 70 mg/dL

26. Although a comatose diabetic patient may
have marked hyperglycemia (with or without
ketoacidosis) rather than hypoglycemia,
these disorders can be distinguished by
estimating blood glucose with a glucose
stick. If this is not available, then glucose
should be given empirically. This will correct
hypoglycemia and will not be particularly
deleterious if the blood glucose
concentration is high.