This document outlines the key points about diabetes mellitus and its acute complications. It begins with definitions of diabetes mellitus and an overview of the different types. The acute complications discussed are diabetic ketoacidosis (DKA), hyperglycemic hyperosmolar nonketotic syndrome (HHNS), and hypoglycemia. For DKA, it covers causes, pathophysiology, signs/symptoms, diagnostic tests, medical management including fluid resuscitation and insulin therapy, and nursing care. HHNS is defined as a hyperglycemic condition without acidosis seen in older patients. Risk factors, signs, and treatment are also summarized.

1. Prepared by:
Miss Ghada Ghazal

2. OUTLINES:
1. DEFINITION OF DIABETES MELLITUS.
2. OVERVIEW OF DIFERRENT TYPE OF D.M.
3. ACUTE COMPLICATION OF DIABETES
MELLITUS THAT REQUIRE EMERGENCY
INTERVENTION.
4. DEFINITION OF
DKA,CAUSES,PATHOPHISIOLOGY,WARNING
SIGN,.CLINICAL MANIFESTATION,MEDICAL
AND NURSING MANAGEMENT.
5. DEFINITION OF HYPERGLYCEMIC
HYPEROSMOLAR NONKETOTIC
SYNDROME,CLINICAL
MANIFESTATION,ASSESSMENT AND
DIAGNOSTIC FINDING,MEDICAL AND NURSING
MANAGEMENT.
6. DEFINITION OF HYPOGLYCEMIA,CLINICAL
MANIFESTATION,AND MANAGEMENT.

3. Diabetes mellitus
• Is a group of metabolic diseases characterized
by elevation levels of glucose in the blood
(hyperglycemia) resulting from defects in insulin
secretion, insulin action, or both.
• D.M is a chronic system disease characterized by
either a deficiency of insulin or decreased ability
of the body to use insulin.

4. TYPE OF D.M:
• 1.insulin dependent D.M.(Type 1 D.M ):is
characterized by destruction of pancreatic beta
cells leading to absolute insulin deficiency ,it
affects 10% of people who have D.M and is
usually diagnosed before the age of 30 years.
• 2.Non insulin dependent D.M:the most
common form of D.M ,it affects 90%to95% of
people who have D.M and is usually diagnosed
after age of 40 years.

5. • 3.Causes of secondary D.M:
• a. Genetic defects.
• b. diseases of the pancreas (such as pancreatitis,
neoplasia)
• c. Drugchemical- indused (as from glucocorticoids,
phenytoin sodium)
• d. Infection (such as congenital rubella, cytomegalovirus
infection)
• e. Endocinopathies (such as acromegaly,
pheochromocytoma, cushings syndrome)
• 4.Gestational diabetes mellitus that occurs during
pregnancy,30%to40% will develop overt D.M (usually
type 2)within 10 years (especially if obese)

6. • Impaired glucose tolerance: oral
glucose tolerance
valuebetween140mg/dl
and200mg/dl.
• Impaired fasting glucose is defined
as a fasting plasma glucose
between 110mg/dl and 126mg/dl.

7. D.M EMERGENCY:
• Acute complication of diabetes mellitus
include:
1.diabeticketoacidosis.
2.Hyperglycemic hyperosmolar nonketotic
syndrome.
3.Hypoglycemia.

8. Diabetic ketoacidosis:
• A metabolic derangement in type one D.M that results
from a deficiency of insulin (anabolic hormone), highly
acidic ketone bodies are formed resulting in acidosis.
• It happen when you have high blood sugar levels and build
up of acids called ketones, if it is not treated ,it can lead to
coma and even death.
• It can also happen with other type of D.M. *
• * DKA is a warning sign that your diabetes is out of control
or that you are getting sick.
• * A serious complication of D.M ,in sufficient insulin levels
in the body result in high blood sugar and the build up of
ketones in the blood.

9. CAUSES OF DKA:
1. Taking too little insulin.
2. Skipping doses of insulin.
3. Inability to meet an increased need for insulin created
by surgery, trauma, pregnancy, stress, and infection.
4. Developing insulin resistance through the presence of
insulin antibodies.
5. Undiagnosed and untreated diabetes.
6. Equipment problem (occlusion of insulin pump tubing)

10. **If you have signs of infection such
as fever, cough, sore throat or pain
when you go to bathroom, contact
your doctor to make sure you are
getting the right treatment.

11. Should I keep taking insulin when
Iam sick?
• Yes, you should keep taking your
insulin even you are too sick to eat
.Your body needs insulin even if you
are not eating. Ask your doctor
whether it is necessary to adjust your
dose or take extra insulin.

12. Pathophisiology:
• DKA is marked by a relative or absolute lack of insulin may
be present ,but not in sufficient amount for the increased
need glucose ,due to the stressors present (infection).
• When the body lacks insulin and cannot use carbohydrates for
energy ,it resorts to using fats and protiens.
• Excess production of counterregularity hormones
(glucagons, catecholamines, cortisol hormones).
Secondary to stress appears to play an important role in the
development of DKA.
• These hormones antagonize the effects of insulin and foster
DKA by promoting hyperglycemia ,osmotic diuresis, lipolysis,
with secondary hyperlipidemia, and acidosis. These hormones
activate hormones-sensitive lipase that increase breakdown of
triglyceride and release of free fatty acids and taken by liver and
converted to ketones body.

13. What are the warning signs of DKA?
1.Vomiting more than once.
2.Epigastric pain, nausea, abdominal pain.
3.Diarrhea,5 or more times in 6 hour.
4.2 blood glucose levels test higher than 300mg/dl.
5.Thirst or very dry mouth.
6.Frequint urination.
7.High levels of ketones in the urine.
8.Dry or flushed skin.
9.Short ,deep breathing, Kassmaul respiration,
(compensatory hyperventilation)

14. • Ketoacidosis is dangerous and
serious, if you have any of above
symptoms, contact your health care
provider immediately or go to the
nearest emergency room.

15. The three clinical features of DKA
are:
1.Hyperglycemia(symptoms of
hyperglycemia includes polyuria, polydipsia
,weight loss, muscle pain and cramp)
2.Dehydration and electrolyte loss.
3.acidosis.

16. ***Symptoms of acidosis and dehydration
includes abdominal pain that may severe
enough to present as surgical emergency
along with vomiting,shortness of
breathing,very deep breathing.kassmaul
respiration(mark of acidosis)
***coma may present in10%of patients.
***bowel sound may be reduced or absent in
severe cases.
***impaired consciousness occurs in
approximately 20% of patients.

17. ****The renal system attempts to excrete enough
ketones body to normalize PH that lead to osmotic
diuresis and hemoconcentration, impedes blood
circulation and causes tissue anoxia, lactic acid
production that increase acidity and decrease PH,
this promote transform of H+ from ECF to ICF.
The movement of hydrogen ions into the cells
promote the movement of K+ out of the cells into
ECF and increase serum K+ level
The client in metabolic acidosis loses excessive
amount of sodium, Ph, Cl, bicarbonate in urine
and vomits.

18. Lab studies:
1. Blood glucose: check blood glucose at least hourly (more frequently if blood
glucose levels fall are made)
2. Blood gases (ABGs): in moderate and severe DKA.PH will be less than 7.2 .It
reflects degree of acidosis by levels of bicarbonates.
3. Potassium: initial blood level usually are normal or high
frequent (every 1_2 hour) check of potassium levels together with ECG monitor.
4. Sodium: measured values are likely to be low because of dilutional effect of
hyperglycemia, osmotic diuresis, water loss. Sodium levels should rises with
treatment.
5. Full blood count: WBC, usually elevated even in the absence of infection.
6. Urine: check all urine for glucose and ketones for at least 24 hour.
7. Perform blood culture and other culture as indicated clinically (urine, throat
swab).
Serum osmolaritry usually elevated.
Lipids: extremely high triglyceride level sometimes present.
***ECG monitor potassium status

19. Characteristic change of hypokalemia
are represented On ECG:
1. prolongation of QT interval.
2. STsegment depression.
3. flat or diphasic T wave.
4. prominant U wave.
5. prolongation of PR interval.
6. sinoatrial block.

20. Hyperkalemia may develop due to over
correction of K+ loss. ECG changes include:
1. broadining of QRS.
2. Peaked T wave.
3. prolonged PR interval.
4. disappearance pf P wave
5. asystole.

21. Critical monitoring(the rehydration
process):
1. Other clinical indices to monitor are tissue turgor , pulse,
condition of mucus membranes, level of consciousness,
thirst, hematocrit and positional blood pressure changes to
check for orthostatic hypotension)
2.For older adults and client with heart disease ,fluid
replacement should be determined according to central
venous pressure measurement.
3.Too aggressive fluid replacement (particularly with normal
saline) may induce heart failure ,frequent auscultation of
the lungs is vital.
4.The best indication of the degree of dehydration is weight
loss ,which may be determined when the clients baseline
weight is known, loss may be 10% of total body weight.

22. Treatment of DKA:
1.Fluid therapy:
a. START with infusion of isotonic saline(,9% sodium
chloride) immediately at rate 15_20ml/kg/hour during the
first hour(1_1.5liters)in the average adult to rapidly expand
the extracellular space.
b. During the second hour: continue fluid as above at
15ml/kg.if the client is hypernatremic ,in heart failure or is
child, consider half strength sodium chloride(,45% normal
saline)
c. During the third hour: reduce fluid intake to7.5 ml/kg in
adults. fluid should be 0,45% normal saline.
d. During the fourth hour: adjust fluid intake to meet clinical
need .consider urine output rate in calculation.

23. **When the blood glucose levels reach 300mg/dl or
less ,the intravenous fluid changed to dextrose
5%in water to prevent hypoglycemia.
* Encourage the client to drink once he or she can
tolerate fluid
* Most client requires urinary catheterization to
monitor urine output
* Patient given0,5-1 liters/hour for first2-3 hours.
* Moderate to high rates of infusion(200-500ml per
hour) may continue to several hours.

24. 2.Restore K+ balance:
because lower PH in un treated DKA ,k+
leave intracellular space and transient
hyperkalemia develops. Correct potassium
replacement requires caution and timely
action intervention begins with fluid and
insulin.
** Dangerous hypokalemia may develop
manifested by general weakness ,extreme
dyspnea that occurs because K+ reenter the
cells (along with glucose) and due to insulin
therapy.

25. ** General agreement exists on the following points
of assessment and intervention:
1. frequently assess and measure urine output .Do
not administer K+ to a client with low urine output
,dangerous hyperkalemia may develop. notify the
physician if urine output decline dramatically or is
less than 0,5 ml/kg/hour.
2. assess the client continuously for evidence of
hyperkalemia (bradycardia, cardiac arrest
,weakness, flaccid paralysis, oliguria )or
hypokalemia (weakness, flaccid paralysis, paralytic
ileus). hyperkalemia may present during the first
four hours of intervention .hypokalemia usually
develops 4to 24 hours after initial intervention.

26. 3.Plan to begin potassium administration with
1-2 hour after starting insulin therapy and
after adequate urine output is ensured.
4.monitor sodium and phosphate level :as with
administration of potassium and insulin
enhances movement of phosphate into the
cells ,which further reduces serum
phosphate level .however, administration of
phosphate can induce hypocalcemia.
Calcium levels should be checked before
phosphate is given.

27. POTASSIUM REPLACEMENT IN
DKA:
** Intravenous replacement of potassium is based on plasma K+
concentration .If K+ concentration is:
a. 3meq/l ,infuse equal or more 0.6mEq/kg/hour.
b. 3-4mEq/l,infuse o.6mEq/kg/hour.
c. 4 -5mEq/l ,infuse 0.2-0.4mEq/kg/hour.
d. 6mEq/l withhold until K+ concentration is <6.0mEq/l
Add K+ to replacement fluid therapy. If concentration 20-40 mEq/l and
infusion into peripheral line causes irritation ,infuse into central line.
Up to 40mEq per hour may be needed for several hours.***
***Initially serum potassium level should be measured every 1-2 hours
because the most rapid change occurs during the first 8 hours of
treatment. After that it should be measured every 4 -6 hours, as
indicated clinically.

28. 3.Correct PH and administration of insulin:
The acidosis that occurs in DKA is reversed with insulin which inhibits fat
breakdown ,there by stopping acid build up .
Insulin is infused intravenously at a slow continuous rate 5units /hourly.,
Hourly blood glucose value must be measured. I.V fluid solution with high
concentration of glucose such as normal saline (D5NS or D50 0.45NS)are
administered when blood glucose level reach 250-300 mg/dl.
Low-dose insulin therapy (5-10 units/hour) is ordered for patient in DKA. The
client with DKA may receive an initial I.V bolus of regular
insulin(0.15units/kg)in the emergency department.
Insulin should never be given subcutaneously to someone in DKA because the
S.C tissue are dehydrated and poorly perfused as a result of dehydration
and hypovolemia.
After the bolus dose given, infuse insulin at rate of 0.1 unit/kg/hour
Example
100 unit of regular insulin are mixed in 500 ml of NS, then 1 unit of
insulin equals 5 ml .Thus an initial insulin pump rate of 5 unit per hour
would equal 25 ml per hour.

29. As the client improves, decision must be made
about discontinue I,V insulin and fluid and begins
subcutaneous insulin administration .Short acting
insulin is administer subcutaneously every 4 -6
hours.
I.V insulin may be continued for 12-24 hour
until the serum bicarbonate level improves to at
least(15-18 mEq/l) and until the patient can eat. In
general bicarbonate infusion to correct severe
acidosis is avoided during treatment of DKA
because it precipitates further, sudden, (and
potentially fatal) decrease in serum potassium
levels. clinicians administer sodium bicarbonates
only to client with a blood PH of 7.1 or less.

30. Nursing management:
Nursing care of the patient with DKA focuses on
monitoring fluid and electrolyte status as well as blood
glucose levels, administering fluids, insulin, and other
medication, and preventing other complication such as
fluid overload .Urine output is monitored to ensure
adequate renal function before potassium is administered
to prevent hyperkalemia. The ECG is monitored for
dysrhythmias indicating abnormal potassium levels. Vital
signs ,arterial blood gases ,and other clinical findings are
recorded on a flow sheet. The nurse document the patient
lab result and the frequent changes in fluids and
medication that are prescribed and monitors the patients
responses.

31. Complication of DKA
The most common complication of DKA are related
to the treatment:
1.Hypoglycemia:due to insulin therapy.
2.Hypokalemia:due to insulin and fluids therapy.
Low potassium levels can impair heart, muscle and
nerve activities.
3.Cerebral edema: is brain swelling caused by a build
up of fluid in the brains cells. It is not certain why
cerebral edema to develop, although it may be
related to rapid fluid replacement.

32. Hyperglycemic ,hyperosmolar
,nonketotic syndrome:
Serious condition in which hyperosmolarity and
hyperglycemia predominate with alteration of
the sense of awareness. A variant of diabetic
ketoacidosis characterized by extreme
hyperglycemia (600-1200mg/dl),profound
dehydration ,mild or undetectable ketonuria and
the absence of acidosis .
HHNS :most commonly occurs in older client
with type 2 D.M

33. Factors associated with HHNS:
1. Therapeutic agent (glucocorticoids, thiazides, diuretics, immunosuppressive
agents)
2. Therapeutic procedure: (peritoneal dialysis, hemodialysis, surgical stress)
3. Chronic illness: (renal disease, heart disease, hypertension, previous stroke)
4. Acute illness: (infection, gangrene, UTI. septicemia, burns, MI, pancreatitis)
**In HHNS the insulin level is too low to prevent hyperglycemia ,and subsequent
osmotic diuresis ,but is high enough to prevent fat breakdown .Patient with
HHNS do not have ketosis related gastrointestinal symptoms that lead them
to seek medical attention .
**In the absence of adequate insulin ,the blood becomes loaded with glucose
,glucose molecules are too large to pass into cells ,therefore osmosis of water
occurs from the interstitial spaces and cells to dilute the glucose in blood
.Osmotic diuresis occurs, eventually the cells become dehydrated .Loss of
water and electrolyte occurs.

34. * Hyperglycemia ,dehydration,
hyperosmolarity may be severe in HHNS.
* Onset is lower (over several days).
* Serum osmolarity >350Osm/l
* Plasma bicarbonates level is normal.
* BUN and creatinine is elevated
* Mortality rate 10% to 40%(clients typically
are older and commonly have significant
medical problem)
* The basic biochemical defect is lack of
effective insulin (like insulin resistance)

35. The following are the four major
clinical features of HHNS
1. Severe hyperglycemia(600-1200 mg/dl)
2. No or only slight ketosis.
3. Profound dehydration(10%to 15% loss of body water)
4. Hyperosmolarity (increased concentration )of plasma
and elevate BUN.
Typically, the client experiences thirst, altered level of
consciousness (coma or confusion) and manifestation
of dehydration (dry mucus membrane, poor skin
turgor), seizures ,hallucination (due to cerebral
dehydration), hypotension, tachycardia (from extreme
hyperosmolarity

36. Medical management:
1. Fluid replacement.
2. Correction of electrolyte and
imbalances.
3. Insulin administration.

37. A common initial intervention is infusion of normal
saline solution(according to sodium level and severity
of volume depletion)over 2-hour period followed by
administration of hypotonic 0.45% saline solution. As
in DKA potassium ,sodium,chloride ,and phosphate are
administered intravenously.
Because of older age of the typical patient with HHNS
,close monitoring of volume and electrolyte status is
important for prevention of fluid overload, heart failure
and cardiac dysrhythmias .Central venous or arterial
pressure monitoring guides fluid replacement.

38. **Potassium is added to the I.V fluid when urine output is
adequate and is guided by continuous ECG monitoring
and frequent laboratory determination.
**Dextrose is added to I.V fluid when the blood glucose level
reaches about 250mg/dl to prevent hypoglycemia .
***Because many clients who have HHNS are older and have
other cardiovascular or renal disorders,fluid volume and
electrolyte changes must be assessed, especially if acute or
chronic renal failure complicates the course.
***Insulin is given via infusion pump ,but usually at lower
dosages and low rate because client is producing some
insulin .Extremely elevated blood glucose drop as the
patient rehydrated.Insulin plays a less important role in the
treatment of HHNS because it is not needed for reversal of
acidosis as in DKA.
***Treatment is continued until metabolic abnormalities are
corrected and neurological symptoms clear,it may take 3 to
5 days for days for neurological symptoms to resolve.

39. Nursing management :
1.Close monitoring of vital signs, fluid status,
laboratory values.
2.Maintain safety and prevent injury related to
changes in the patient neurological status .
3.Monitor urine output closely (high risk for
renal failure due to severe dehydration)

40. Hypoglycemia:
Is a common feature of type one diabetes mellitus
can also be seen in clients with type 2 D.M
treated with insulin or oral agents.
Usually do not occur until the blood glucose is less
than 50 to 60 mg/dl (2.7 to 3.3 mmol/l).

41. Etiology and risk factor:
1.An over dose of insulin or less commonly a sulfonylurea.
2.Omitting a meal or less food than usual.
3.Over excretion without additional carbohydrate compensation.
4.Nutrition and fluid imbalances caused by nausea and vomiting
5.Alcohol intake.
6.Vigorous unexpected exercise.
* It occurs before meals ,especially if meals are delayed or
snacks are omitted.
* Clients at risk for hypoglycemia while taking an oral
hypoglycemic agents are older than age of 60 years, have
poor nutritional intake ,have hepatic or renal dysfunction.

42. Clinical manifestation:
1.Adrenergic(increased epinephrine) occurs in mild hypoglycemia.
Shakiness,irritability,nervousness,tachycardia,palpitation,tremor,hun
ger,diaphrosis,pallor,paresthesia.
2.Neuroglycopenic (decreased glucose to brain)occurs in moderate
to severe hypoglycemia.
Headache ,mental illness, inability to concentrate, slurred speech,
blurred vision, confusion, lethargy, loss of consciousness, coma,
seizure, death.
***Hypoglycemia can occurs at any time of day or night , it
seems to occur most frequently during exercise, in the
middle of the night. Severe hypoglycemia seems to occur
more often in the people who have hypoglycemic
unawareness , defective glucose counter regulation, and
autonomic neuropathy.

43. Assessment and diagnostic finding:
Symptoms can occur suddenly and unexpectededly .The
combination of symptoms varies from person to
person.
Patient who usually have a blood glucose level in the
hyperglycemic range (eg. in the 200sor greater) feel
hypoglycemic (adrenergic symptoms) when their blood
glucose quickly drops to 120mg/dl or less, conversely
patient who frequently have a glucose level in the low
range of normal may be asymptomatic when the blood
glucose slowly falls to less than 50mg/dl.

44. Medical management:
Management depends on the severity of the reaction.
Initiating emergency measure: for patient who are
unconscious and can not swallowed ,an injection of
glucagon 1mg can be administered either S.C or I.M
(hormone produced by the alpha cells of the pancreas
that stimulate liver to release glucose. Injectable
glucagon is packaged as a powder in 1 mg vial and most
be mixed with diluent before being injected. After
injection of glucagon ,it may take up to 20 min for the
patient to regain consciousness.
Duration of the action of 1mg glucagon is brief its onset
is 8-to 10 min and its action lasts 12-to 27 min. Nausea
is the major side effect that occurs after injection of
glucagon.

45. • Patient who are unconscious or can not
swallow may be treated with 25 to 50 ml of
50% dextrose in water or 10-25gm of dextrose
50% administered I.V over 1 to 3 min .This is
followed by an infusion of 5% dextrose at 5-
10ml/hour until the client is fully recovered and
able to eat.. Assuring patency of the I.V line
used for injection of 5% dextrose is essential
because hypertonic solution 50%dextrose are
very irritating to the veins.

46. Never force an unconscious or semiconscious
client to drink liquid ,because fluid may be
aspirated to the lung.
Mild hypoglycemia:
Intervention:10-15g of carbohydrates contained
in the following:(4 oz orange juice,6 oz regular
soda,6-8 oz 2%milk,4 tsp granulated sugar)
Moderate hypoglycemia:20-30 g of
carbohydrates.Glucagon ,1 mg S.C or I.M.
Severe hypoglycemia:50%dextrose,25 g
I.V.Glucagon ,1 mg I.M or I.V.***