3. objectives
At the end of this seminar students are expected
to:
have a general view of diabetes
define what a DKA is
understand the pathophysiology of DKA
know basics of approach to a patient with DKA
manage a patient with DKA
4. Introduction
Diabetes Mellitus: is a common endocrine
disorder characterized by:
Hyperglycemia
Manifesting often with symptoms and signs of
osmotic diuresis such as polyuria and polydypsia
Calorie loss, generalized weakness, polyphagia
and weight loss.
5. Classification
Type 1 (beta cell destruction, usually leading to absolute insulin
deficiency)
Type 2 (may range from predominantly insulin resistance with relative
insulin deficiency to a predominantly insulin secretory defect with
insulin resistance)
Other specific type
A. Genetic defects of beta cell function characterized by mutations in:
B. Genetic defects in insulin action.
C .Diseases of the exocrine pancreas.
D .Endocrinopathies
E.Drug
F.Infections
G.Uncommon forms of immune-mediated diabetes— "stiff-person
Syndrom”
GDM
6. Epidemiology
The worldwide prevalence of DM has risen
dramatically over the past two decades, from an
estimated 30 million cases in 1985 to 285 million in
2010.
Based on current trends, the International
Diabetes Federation projects that 438 million
individuals will have diabetes by the year 2030
7. Although the prevalence of both type 1 and type
2 DM is increasing worldwide,
The prevalence of type 2 DM is rising much more
rapidly, presumably because of
increasing obesity,
reduced activity levels as countries become more
industrialized, and
the aging of the population.
9. Chronic complication
Microvascular
Macrovascular Other
Eye disease Coronary heart disease Gastrointestinal
(gastroparesis, diarrhea)
Retinopathy
(nonproliferative/prolifer
ative)
Peripheral arterial
disease
Genitourinary
(uropathy/sexual
dysfunction)
Macular edema Cerebrovascular
disease
Dermatologic
Neuropathy Infectious
Sensory and motor
(mono- and
polyneuropathy)
Cataracts
Autonomic Glaucoma
Nephropathy Periodontal disease
Hearing loss
10. Diabetic ketoacidosis
The most frequent endocrine emergency seen by
the primary care physician
May be the 1st
presentation of type 1 DM
Result from absolute insulin deficiency or increase
requirement
11. three cardinal biochemical features of
DKA:
Hyperglycemia
Ketosis
Acidosis
Results from:
hormonal imbalance
Insulin deficiency
Excessive counter-regulatory hormones
12. Precipitating causes for
DKA
Lack of insuline/ drug omission most common PPt factor
Infection chest(TB, pneumonia), UTI
Trauma
infarction
inadequate food intake and
skipping of injection
reduction in the dose of insulin
severe emotional stress
23. Treatment of DKA
Aims of treatment
Fluid replacement
Electrolyte correction
Acidosis correction
Insulin therapy for
hyperglycemia
Treatment of ppt cause
24. 1. Confirm diagnosis (plasma glucose, positive serum ketones,
metabolic acidosis).
2. Admit to hospital; intensive-care setting may be necessary for
frequent monitoring or if pH <7.00 or unconscious.
3. Assess:
Serum electrolytes (K+
, Na+
, Mg2+
, Cl–
, bicarbonate, phosphate)
Acid-base status—pH, HCO3
–
, PCO2, -hydroxybutyrate
Renal function (creatinine, urine output)
25. 4. Replace fluids: 2–3 L of 0.9% saline over first 1–3 h ? (15–20
mL/kg per hour),
subsequently, 0.45% saline at 250–500 mL/h;
change to 5% glucose and 0.45% saline at 150–250 mL/h
when plasma glucose reaches 200 mg/dL
5. Administer short-acting insulin: IV (0.1 units/kg),
then 0.1 units/kg per hour by continuous IV infusion; increase
two- to threefold if no response by 2–4 h.
If the initial serum potassium is <3.3 meq/L, do not administer
insulin until the potassium is corrected.
If the initial serum potassium is >5.2 meq/L, do not supplement K+
until the potassium is corrected.
26. 6. Assess patient: What precipitated the episode
noncompliance
infection
trauma
infarction and
cocaine
Initiate appropriate workup for precipitating
event(cultures,CXR, ECG).
7. Measure
capillary glucose every 1–2 h;
measure electrolytes (especially K+
, bicarbonate,
phosphate) and anion gap every 4 h for first 24 h.
28. DKA management
protocol
General measures
Stabilize ABC of life
Obtain iv access
Put them on cardiac monitor control if available
Monitor RBS every hour,urine ketone every four
hour,vital signs Q2-4hr.
Identify and treat precipitating cause.
29. Replete fluid deficit
Give as much as NS rapidly for a patient in shock
Give at least 3 bags of NS in the first 3-4hrs unless
there is acardiac compromise.
Change toDNS when blood sugar fall below 200
Replace ongoing fluid loss
The usual fluid deficit is about 3-6 litter
30. Replet K deficit
If baseline kis <3.3mEq/l avoid insulin and administer 20-
30mEq/l per hour until k is above 3.3mEq/l
If baseline k is 3.3-5.3 mEq/l or is unkown administer 40mEq/l
to run over 4-8hr after conofirming adequate urine
output(≥50ml/hr or give po kcl)
if baseline k is above 5.3mEq/l don’t administer k
The target is to keep it b/n 4-5mEq/l
The k should be supplemented by second iv line not to
compromise the fluid resuscitation
If abaseline serum k is unknown do ECG and check signs of
hypo or hyperkalemia
31. Give insulin
Give initial bolus of 10iu iv and 10iu im of regular insulin
Then give 5iu iv every 1hr until blood sugar <200mg/dl and ketone urine
twice negative
If blood sugar doesn’t drop or is persistently above 350-400mg/dl double the
dose of insulin
Overlap the last dose with the standing dose of long acting insulin
In pts with known DM who where previously treated with insulin may be
given the same dose they were given before
For newly diagnosed pts insulin should be started at dose of 0.5-0.8
iu/kg/day
Measure RBS every 4-6hrs aday and give correctional dose of regular
insulin(1-2iu for every 50mg/dl rise above 200mg/dl)
32. Patient education
Advise on adherence and appropriate storage of
insulin
Advise on what to do when they have poly
symptom and other symptoms of DKA
Advise on self monitoring of blood sugar
34. Introduction
Extremely high blood glucose level (600-
2000 mg/dL)
Absence of or small amounts of ketones
Profound dehydration
Pts have sufficient insulin to prevent
lipolysis and ketosis
Occurs in older patients with type 2
diabetes
Treatment: hydration and small doses of
insulin to correct the hyperglycemia
34
35. Clinical Features
Symptoms
a several-week history of polyuria
weight loss, and
diminished oral intake that culminates in
mental confusion,
lethargy, or coma.
35
37. precipitated by
HHS is often precipitated by a serious, concurrent
illness such as
myocardial infarction or
stroke.
prior stroke or
Dementia
Pneumonia
sepsis
37
38. Laboratory Abnormalities and Diagnosis
plasma glucose may be >55.5 mmol/L (1000
mg/dL)],
hyperosmolality (>350 mosmol/L)
prerenal azotemia
The measured serum sodium may be normal or
slightly low despite the marked hyperglycemia.
38
39. The corrected serum sodium is usually increased
[add 1.6 meq to measured sodium for each 5.6-
mmol/L (100 mg/dL) rise in the serum glucose].
In contrast to DKA,
acidosis and ketonemia are absent or mild.
39
40. A small anion-gap metabolic acidosis.
Moderate ketonuria.
40
42. Treatment: Hyperglycemic
Hyperosmolar State
Treatment involves
• Fluid replacement : administration of IV fluids and
• Bringing down the blood sugar rapidly by using
rapidly acting insulin preparations
• Identifying and treating the precipitating factor
42
43. Underlying or precipitating problems should be
aggressively sought and treated.
In HHS, fluid losses and
dehydration are usually more pronounced than in
DKA.
due to the longer duration of the illness.
43
44. The patient with HHS is usually
older, more likely to have mental status changes,
and
more likely to have a life-threatening
precipitating event with accompanying
comorbidities.
Even with proper treatment, HHS has a
substantially higher mortality rate than DKA (up to
15% in some clinical series).
44
45. Fluid replacement
Fluid replacement should initially stabilize the
hemodynamic status of the patient (1–3 L of 0.9%
normal saline over the first 2–3 h).
Because the fluid deficit in HHS is accumulated
over a period of days to weeks, the rapidity of
reversal of the hyperosmolar state
must balance the need for free water repletion
with the risk that too rapid a reversal may worsen
neurologic function.
45
46. If the serum sodium > 150 mmol/L (150 meq/L),
0.45% saline should be used.
After hemodynamic stability is achieved,
the IV fluid administration is directed at reversing
the free water deficit using hypotonic fluids
(0.45% saline initially, then 5% dextrose in water,
D5W).
46
47. calculated free water deficit
(which averages 9–10 L) should be reversed over
the next 1–2 days
(infusion rates of 200–300 mL/h of hypotonic
solution).
47
48. Insulin
As in DKA, rehydration and volume expansion
lower the plasma glucose initially,
but insulin is also required.
A reasonable regimen for HHS begins with an IV
insulin bolus of 0.1 units/kg
followed by IV insulin at a constant infusion rate
of 0.1 units/kg per hour.
48
49. . If the serum glucose does not fall, increase the
insulin infusion rate by twofold.
As in DKA, glucose should be added to IV fluid
when the plasma glucose falls to 13.9–16.7
mmol/L (250–300 mg/dL), and
the insulin infusion rate should be decreased to
0.05–0.1 units/kg per hour.
49
50. The insulin infusion should be continued until the
patient has resumed eating and can be
transferred to a SC insulin regimen.
The patient should be discharged from the
hospital on insulin, though some patients can later
switch to oral glucose-lowering agents.
50
51. A 62 year-old man is brought to the emergency department
by his family because he is confused. His wife had not noticed
any fever,chills,nausia or vomiting.
He appears very lethargic, he is arousable but responds
incoherently to questions. He only orient to his home.
T:98.9 F BP:102/62 mmHg P:122/min RR:18/min
His lung examinations is normal. His heart has RRR. There are
no focal neurologic signs. And The reast of his PE is
unremarkable.
51
52. Lab
-Glucose 1,118mg/dl
-K 4.8 mg/dl
-BUN 61, Creatinine 1.5mg/dl
Hco3 24meq/l
Na 130mg/dl
CL 100 mg/dl
Ketones negatives
ECG no IHD
Chest x ray P
UA P
52
53. Admit ICU
Aggressive IVF 0.9 NS
Insulin IV then IM
EcG
Blood and urine cultures etc
53
55. introduction
Hypoglycemia is defined as all episodes of
an abnormally low plasma glucose
concentration (with or without symptoms)
that expose the individual to harm.
Hypoglycemia is a clinical syndrome of
diverse causes in which low levels of
serum glucose can eventually lead to
neuroglycopenia.
55
56. Clinical classification
Severe hypoglycemia:An event requiring the
assistance of another person to actively administer
carbohydrate, glucagon or other resuscitative
actions is classified as a severe hypoglycemic
event.
Documented symptomatic hypoglycemia : An
event during which typical symptoms of
hypoglycemia are accompanied by a measured
(typically with a monitor or with a validated
glucose sensor) plasma glucose concentration ≤70
mg/dL (3.9 mmol/L) is classified as a documented
symptomatic hypoglycemic event.
56
57. Cont’d……….
Asymptomatic hypoglycemia : Asymptomatic
hypoglycemia is classified as an event not
accompanied by typical symptoms of
hypoglycemia but with a measured plasma
glucose concentration of ≤70 mg/dL (3.9
mmol/L).
Probable symptomatic hypoglycemia : Probable
symptomatic hypoglycemia is classified as an
event during which typical symptoms of
hypoglycemia are not accompanied by a plasma
glucose determination (but that was presumably
caused by a plasma glucose concentration ≤70
mg/dL [3.9 mmol/L]).
57
58. Cont’d….
Relative hypoglycemia: Relative
hypoglycemia is classified as an event
during which the person with diabetes
reports typical symptoms of hypoglycemia,
and interprets those as indicative of
hypoglycemia, but with a measured plasma
glucose concentration >70 mg/dL (3.9
mmol/L).
58
59. Impact and Frequency
Hypoglycemia is the limiting factor in the
glycemic management of diabetes.
Hypoglycemia is a fact of life for people with
T1DM.
They suffer an average of two episodes of
symptomatic hypoglycemia per week and at
least one episode of severe, at least
temporarily disabling, hypoglycemia each
year.
An estimated 6–10% of people with T1DM
die as a result of hypoglycemia
59
60. Cont’d……..
Hypoglycemia occurs less frequently in
T2DM.
The frequency of hypoglycemia
approaches that in T1DM as persons with
T2DM develop absolute insulin deficiency
and require more complex treatment with
insulin.
60
61. Conventional Risk Factors
Insulin (or insulin secretagogue) doses are
excessive, ill-timed, or of the wrong type.
The influx of exogenous glucose is reduced
(e.g., during an overnight fast or following
missed meals or snacks.
Insulin-independent glucose utilization is
increased (e.g., during exercise).
Sensitivity to insulin is increased (e.g., with
improved glycemic control, in the middle of
the night, late after exercise, or with increased
fitness or weight loss).
61
62. CONT’D………
Endogenous glucose production is reduced
(e.g., following alcohol ingestion).
insulin clearance is reduced (e.g.,
in renal failure).
62
63. Causes of Hypoglycemia
Drugs: Insulin or insulin secretagogue, Alcohol,
Others.
Critical illness: Hepatic, renal or cardiac failure,
Sepsis , Inanition
Hormone deficiency: Cortisol, Glucagon and
epinephrine (in insulin-deficient diabetes)
Non–islet cell tumor: Seemingly well individual
Endogenous
hyperinsulinism : Insulinoma , Functional beta-cell
disorders (nesidioblastosis)
Accidental, surreptitious or malicious hypoglycemia
63
64. Table 345-2 Physiologic Responses to Decreasing Plasma Glucose
Concentrations
Response Glycemic Threshold,
mmol/L (mg/dL)
Physiologic Effects Role in the Prevention or
Correction of
Hypoglycemia (Glucose
Counterregulation)
↓Insulin 4.4–4.7 (80–85) ↑Ra (↓ Rd)
Primary glucose
regulatory factor/first
defense against
hypoglycemia
↑Glucagon 3.6–3.9 (65–70) ↑Ra
Primary glucose
counterregulatory
factor/second defense
against hypoglycemia
↑EPINEPHRINE 3.6–3.9 (65–70) ↑Ra, ↓Rc
Third defense against
hypoglycemia, critical
when glucagon is
deficient
↑GROWTH
HORMONEAND
CORTISOL
3.6–3.9 (65–70) ↑Ra,↓ Rc
Involved in defense
against prolonged
hypoglycemia, not critical
SYMPTOMS 2.8–3.1 (50–55) Recognition of
hypoglycemia
Prompt behavioral
defense against
hypoglycemia (food
ingestion)
↓COGNITION <2.8 (<50) (Compromises behavioral
64
65. Hypoglycemia in insulin-treated patients
with diabetes occurs as a consequence
of three factors:
Behavioral issues
Impaired counterregulatory systems
Complications of diabetes.
65
69. Approach to the Patient:
Hypoglycemia
In addition to recognition and
documentation of hypoglycemia, and often
urgent treatment, diagnosis of the
hypoglycemic mechanism is critical for
choosing a treatment that prevents, or at
least minimizes, recurrent hypoglycemia.
69
70. Recognition and Documentation
Hypoglycemia is suspected: in patients with typical
symptoms; in the presence of confusion, an altered level of
consciousness, or a seizure; or in a clinical setting in which
hypoglycemia is known to occur.
low plasma glucose concentration.
Whipple's triad
70
71. When the cause of the
hypoglycemic episode is obscure:
plasma insulin, C-peptide, proinsulin
As well as screening for circulating oral
hypoglycemic agents, and symptoms should be
assessed during and after the plasma glucose
concentration is raised.
71
72. Diagnosis of the Hypoglycemic
Mechanism
In a patient with documented hypoglycemia, a
plausible hypoglycemic mechanism can often
be deduced from the history, physical
examination, and available laboratory data.
first consideration: Drugs, particularly
those used to treat diabetes or
alcohol.
Other considerations : include evidence
of a relevant critical illness, less
commonly hormone deficiencies, and
rarely a non–beta-cell tumor that can
be pursued diagnostically.
72
73. CONT’D……
Absent one of these mechanisms, in an
otherwise seemingly well individual, one
should consider endogenous
hyperinsulinism and proceed with
measurements and assessment of
symptoms during spontaneous
hypoglycemia or under conditions that
might elicit hypoglycemia.
73
74. Urgent Treatment
Oral treatment with glucose tablets or glucose-
containing fluids, candy, or food is
appropriate if the patient is able and willing to
take these. A reasonable initial dose is 20 g of
glucose.
Intravenous glucose (25 g) should be given
and followed by a glucose infusion guided by
serial plasma glucose measurements.
If intravenous therapy is not practical,
subcutaneous or intramuscular glucagon (1.0
mg in adults) can be used, particularly in
patients with T1DM.
74
75. CONT’D….
These treatments raise plasma glucose
concentrations only transiently,
and patients should therefore be urged to eat as
soon as is practical to replete glycogen stores.
75
76. MEASURES FOR AVOIDANCE AND
TREATMENT OF HYPOGLYCAEMIA
DURING TRAVEL
Carry supply of fast-acting carbohydrate (non-
perishable, in suitable containers):
Screwtop plastic bottles for glucose drinks
Packets of powdered glucose (for use in hot, humid
climates).
Confectionery (foil wrapping in hot climates).
Companions should carry additional oral
carbohydrate, and glucagon .
Frequent blood glucose testing (carry spare meter;
visually read strips).
Use fast-acting insulin analogues for long-distance air
travel.
76
77. Prevention of Recurrent
Hypoglycemia
Prevention of recurrent hypoglycemia requires an
understanding of the hypoglycemic mechanism.
Offending drugs can be discontinued or their
doses reduced.
Cortisol and growth hormone can be replaced if
they are deficient.
Surgical resection of an insulinoma is curative;
medical therapy with diazoxide or octreotide can
be used if resection is not possible and in patients
with a nontumor beta-cell disorder.
77
78. Cont’d………….
Surgical, radiotherapeutic,or chemotherapeutic reduction of
a nonislet cell tumor can alleviate hypoglycemia even if the
tumor cannot be cured; glucocorticoid or growth hormone
administration also may reduce hypoglycemic episodes in
such patients.
78
79. complications
recurrent/persistent psychosocial morbidity
Fear of hypoglycemia-barrier for diabetic control.
Seizure
permanent neurologic deficit (including cognitive
impairment)
Coma
Death
79
Dx of DKA: hyperglycemia, ketosis (serum not urine), Acidosis PH&lt;7.3
+251925913947Abrham.S
ECG features of hyperkalemia
5.5-6.5 Tall peaked T waves
6.5-7.5 Loss of P waves
7.0-8.0 Widening of QRS complexes
8.0-10 Sine wave, ventricular arrhythmias, asystole
Electrocardiographic features of hypokalaemia
Broad, flat T waves
ST depression
QT interval prolongation
Ventricular arrhythmias (premature ventricular contractions, torsades de pointes, ventricular tachycardia, ventricular fibrillation)
