ACUTE BIOLOGICAL

CRISIS

ACUTE COMPLICATIONS
OF DIABETES MELLITUS
Hyperglycemia and Diabetic
Ketoacidosis

Hyperglycemia results when

glucose cannot be
transported to the cells
because of a lack of insulin
The liver converts its
glycogen stores back to
glucose (glycogenolysis) and
increases the biosynthesis of
glucose (gluconeogenesis)
In type I DM, as the need for
cellular fuel grows more
critical, the body begins to
draw its fat and protein stores
for energy
The liver, in turn, accelerates
the rate at which it produces
ketone bodies (ketogenesis)
for catabolism by other
tissues, particularly muscle
As fat metabolism increases,
the liver may produce too
many ketone bodies
Ketone bodies accumulate in
the blood (ketosis) and are
excreted in the urine
(ketonuria)

Metabolic acidosis develops

from the acidic (pHlowering) effect of the
ketones acetoacetate and
beta-hydroxybutyrate
This condition is called
DIABETIC
KETOACIDOSIS
Severe acidosis may cause
the diabetic client to lose
consciousness, a condition
often called DIABETIC
COMA

insulin due to
surgery, trauma,
pregnancy, stress,
puberty, or infections
d. Developing insulin
resistance as a result
of the presence of
insulin antibodies
PATHOPHYSIOLOGY

Relative or absolute lack of

insulin

Increased need of glucose

due to stressors present (e.g.,
infections)

Use of fats and proteins for

energy

What is DKA?

DKA is always a medical

emergency and requires
immediate medical attention

has a fruity or acetone-like

odor
Renal system tries to excrete
ketones that leads to osmotic
diuresis and
hemoconcentration
Hemoconcentration impedes
blood circulation and leads to
tissue anoxia and lactic acid
production
The rising ketone bodies
overwhelms the bodys
defenses against hydrogen
excess, the body finally
succumbs to acid overload,
and diabetic coma can ensue
DEHYDRATION

DKA is the most serious

metabolic disturbance of type
I DM

Occurs most frequently in

teenagers and the elderly

Etiology and Risk Factors

Primarily a complication of
type I DM, although clients
with NIDDM can also
develop ketoacidosis during
periods of extreme stress

Common causes:
a. Taking too little
insulin
b. Omitting doses of
insulin
c. Failing to meet an
increased need for

Excess counterregulatory
hormones (glucagon,
catecholamines, cortisol, and
growth hormones) secondary
to stress
Hormones antagonize the
effects of insulin and DKA
by promoting hyperglycemia,
osmotic diuresis, lipolysis
with secondary
hyperlipidemia, and acidosis
The processes of catabolizing
fats for fuel gives rise to:
KETOSIS
Respirations increase in rate
and depth (Kussmauls
respirations) and the breath

Diuresis
Nausea and vomiting
(loss of sodium and
chloride)
Water loss in breath
Followed by
hypovolemic shock and
lactic acidosis

ELECTROLYTE
IMBALANCE
Hydrogen moving into the cell leads
to severe intracellular potassium
depletion
Osmotic diuresis leads to more
potassium excreted

 Client in metabolic
acidosis loses excessive
amounts of sodium,
phosphate, chloride, and
bicarbonate in the urine
and vomitus

CLINICAL MANIFESTATIONS
Signs
Tachycardia
Hypotension
Dehydration
Ward, dry skin
Hyperpnea or Kussmauls
respirations
Impaired level of
consciousness or coma
Weight loss
Fruity odor of ketones on
breath
Symptoms
Nausea and vomiting
Thirst and polyuria
Weakness and/or anorexia
Abdominal pain
Visual disturbances
Somnolence
MANAGEMENT
Rehydration (0.9% sodium
chloride)
1,000 ml during the first
hour (10 to 20 ml/kg)
Followed by 2,000 to 8,000
ml of solution over the next
24 hours
Clients with compromised
CV function may require
slower IV fluid replacement

NGT to prevent
aspiration (frequent oral
care)
Encourage fluid when
able to tolerate (salted
broth to replace sodium)
I and O monitoring (use
catheters)

Reversing shock

May order blood,

albumin, or other plasma
volume expanders such as
dextran

Restoring potassium balance

pH correction / Insulin
Administration
Blood glucose level
need to be monitored
frequently

THYROID STORM
(THYROTOXICOSIS)

A potentially fatal, acute

episode of thyroid
overactivity characterized by
high fever, severe tachycardia,
delirium, dehydration, and
extreme irritability

Thyroid storm is a clinical

diagnosis; no laboratory tests
serve to differentiate
hyperthyroidism from thyroid
storm in general

It is an emergency and
requires heroic intervention
for control
Precipitating factors include:
Undiagnosed or untreated
hyperthyroidism
Infection
Thyroid ablation
Metabolic catastrophes
Surgery
Trauma
Labor and delivery
MI
Pulmonary embolus
Medication over dosage
Inadequate preparation of
clients for thyroid surgery

PREVENTION

Take insulin in appropriate

doses at appropriate times
Monitor blood glucose levels
frequently (at least before
each meal and at bedtime)
Monitor urine ketone levels
when blood glucose levels
rise (above 250 mg/dl)
Schedule regular
appointments with the
healthcare provider
Recognize manifestations of
infection

MANAGEMENT

High fever is treated with

hypothermic blankets
Dehydration is reversed with
IV fluids

Suppress the hormone

release:
Inhibiting hormonal
synthesis
Blocking conversion of T4
to T3
Inhibiting the effects of TH
on body tissues as well as
treating the precipitating
factors

Blockade of TH release is
usually achieved by the
administration by the
administration of iodides
such as potassium iodide
given orally

Sodium iodide may be given

IV

Glucocorticoid,
dexamethasone, and
propylthiouracil are also
commonly used oral drugs

Beta-blockers are given to

decrease the effects of
sympathetic and treat
tachycardia

SHOCK

Complex clinical syndrome

that may occur at any time
and in any place
It is a life-threatening
condition often requiring
team action by many
healthcare providers
Defined as a failure of the
circulatory system to
maintain adequate perfusion
of vital organs

Major classifications

Hypovolemic shock due to

inadequate circulating blood
volume resulting from
hemorrhage with actual
blood loss, burns with loss of
plasma proteins and fluid
shifts, or dehydration with a
loss of fluid volume
Cardiogenic shock due to
inadequate pumping action
of the heart because of
primary cardiac muscle
dysfunction or mechanical
obstruction of blood flow
caused by MI, valvular
insufficiency due to disease
or trauma, cardiac
dysrhythmias, or an
obstructive condition, such
as pericardial tamponade, or
pulmonary embolus
Distributive shock due to
changes in blood vessel tone
that increase the size of the

vascular space without in

increase in the circulating
blood volume
Further divided into:
Anaphylactic shock
severe hypersensitivity
reaction resulting in
massive vasodilation

Neurogenic shock
interference with nervous
system control of the
blood vessels (SCI)

Septic shock due to

release of vasoactive
substances

ETIOLOGY AND RISK

FACTORS

Cardiogenic shock
Myocardial infarction
Impaired myocardial
contractility may also occur
with blunt cardiac trauma,
cardiomyopathy, and CHF
Obstructive conditions
Large pulmonary
embolism, pericardial
tamponade, and tension
pneumothorax

Insufficient quantity of blood

(hypovolemic)

Incompetent pump
(cardiogenic shock)

Ineffective delivery of blood

(distributive shock)

Other causes
Cardiac valvular
deficiency, myocardial
aneurysms, rupture of
valvular papillary muscle,
rupture of a ventricle,
aortic stenosis, mitral
regurgitation, and cardiac
dysrhythmias

Hypovolemic shock
Hemorrhage
Blood volume deficit of
15% to 25%, or about 500
to 1,500 ml in an adult
with a normal circulating
volume
Burns
Occurs with large partialthickness or full-thickness
burns

May also have

cardiac dysfunction
due to MDF
Dehydration
Occurs from either
reduced oral fluid
intake or significant
losses of fluid

Spinal Cord Injury

(Neurogenic shock)

Infection (Septic shock)

PATHOPHYSIOLOGY

Interrelated components of
the cardiovascular system:
Heart
Vascular tone
Blood volume

Heart and brain are the

organs considered vital to
survival. GIT, skin, muscle,
and kidneys are not
considered by the body as
vital to survival

RAAS

MAP should be 70-105

mmHg
MAP = (systolic + [2 x
diastolic[) / 3
STAGES OF SHOCK

1. Early Compensation stage

2. Decompensation stage
3. Progressive stage

Distributive shock
Systemic affects of shock

Acute Allergic Reaction

(anaphylactic shock)
Penicillin, penicillin
derivatives, bee stings,
chocolate, strawberries,
peanuts, snake venom,
iodine-based contrast for xrays, foods and NSAIDs

Respiratory system
Acid-Base balance
Cardiovascular system
Myocardial
deterioration
DIC
Vasoconstriction

Neuroendocrine system
Adrenal response
Pituitary response
Metabolic response
Neurologic response

Effects on Immune system

Effects on GI system
Effects on Renal system

General Clinical Manifestations of

Shock

Tachypnea
Tachycardia
Hypotension
Changes in LOC
Oliguria

Medical Management

Maintaining adequate
perfusion
Vasoconstrictors
Vasodilators
Improving oxygenation
Assisting circulation
MAST Garment
Intra-aortic balloon
pump
Modified
Trendelenburgs
position
Replacing fluid volume
Crystalloid or
Balance Salt
Solution
Colloid solutions
Blood
Providing autotransfusion
Evaluating Fluid replacement

Providing pharmacologic
Management
Monitoring Urine Output
Preventing GI bleeding

Nursing Management

Assessment
Non invasive
techniques (ABC)
Blood Pressure
monitoring
Invasive techniques
(CVP)
Diagnosis
Evaluation