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Metabolic Emergencies
Diabetic Ketoacidosis
Melanie S. Banaticla, RN,MAN
Diabetic ketoacidosis (DKA)
• DKA occurs predominantly in patients with
Type 1 diabetes, but has been known to rarely
occur in those with Type 2, typically in the
presence of a coexisting acute illness
Diabetic Ketoacidosis
• Caused by an absence or markedly inadequate
amount of insulin.
• This results in disorders in the metabolism of
carbohydrate, protein, & fat
• Three main clinical features are:
– Dehydration
– Electrolyte loss
– acidosis
• It is an acute, life-threatening emergency
associated with very high serum glucose levels
and no insulin.
• Due to the lack of insulin the body’s cells begin to
starve, and after two or three days the body
starts breaking down adipose tissue and proteins
in an attempt to produce a usable energy source.
This process is known as glyconeogenesis. The
by-product of this process is an acid referred to as
• The increase in circulating acids causes blood pH
to fall leading to metabolic acidosis.
When INSULIN is lacking…
• The amount of glucose entering the cells is
reduced. In addition, there is unrestrained
production of glucose by the liver.
• These lead to HYPERGLYCEMIA.
• In an attempt to rid the body of excess glucose,
the kidneys excrete the glucose along with water
& electrolytes (Na & K).
• This osmotic diuresis, characterized by polyuria
leads to dehydration & marked electrolyte loss.
• Patients with severe DKA may lose an average
of 6.5 L of water & up to 400-500 mEq each of
Na, K, & Chloride over 24 hour period.
Another effect of INSULIN deficiency
• Breakdown of fat (lipolysis) into free fatty acids &
• The free fatty acids are converted into ketones
bodies by the liver.
• In DKA there is an excess production of ketone
bodies because of lack of insulin (that would
normally prevent this from occuring).
• KETONE BODIES are acids, & when they
accumulate in the circulation they lead to
Signs & Symptoms
• Hyperglycemia leads to polyuria & polydipsia
(increased thirst)
– Blurred vision, weakness, & headache
– Orthostatic hypotension
– Weak, rapid pulse
Signs & Symptoms
• The ketosis & acidosis characteristic of DKA
lead to gastrointestinal symptoms such as:
• Anorexia, n/v, & abdominal pain
• Acetone breath (fruity odor) – occurs with
elevated levels of ketone bodies.
• Hyperventilation (kussmaul respiration) to
decrease acidosis
• Mental status may vary, may be alert,
lethargic, or comatose
Kussmaul Breathing
• abnormally slow deep respiration
characteristic of air hunger & occuring
especially in acidotic states.
Abnormal metabolism that causes s/sx of diabetic
Insulin lack
↑Breakdown of fat
↓Glucose utilization by the
muscle, fat & liver
↑Fatty acids
↑Glucose production by
Blurred vision
↑ketone bodies
Evidence of ketoacidosis
• Low serum bicarbonate (0-15 mEq/L)
• Low pH (6.8 to 7.3)
• Low pCO2 (10-30 mm Hg) – reflects
respiratory compensation (kussmaul
respiration)for metabolic acidosis
• Accumulation of ketone bodies is reflected in
blood & urine ketone measurements.
3 main causes of DKA
• 1. A decreased or missed dose of insulin
• 2. An illness or infection – are associated with
insulin resistance.
• In response to physical & emotional stresses, there is an
increase in the level of “stress” hormones – glucagon,
epinephrine, norepinephrine, cortisol, & growth hormone.
• These hormones promote GLUCOSE PRODUCTION by the
liver & interfere with glucose utilization by muscle & fat
tissue, counteracting the effect of insulin.
• 3. The initial manifestation of undiagnosed &
untreated diabetes
• Aimed at correction of the three main
– Dehydration (rehydration)
– Electrolyte loss (K infusion)
– Acidosis ( insulin drip)
For safe infusion of K, the nurse should
check that:
• There are no signs of hyperkalemia on the ECG
(tall, peaked T waves)
• The laboratory values of K are normal or low
(N-4-4.5 mmol/L)
• The patient is urinating (i.e, not experiencing
renal shutdown)
Prevention & Education
“sick day rules” for managing DM
when ill
Guidelines to follow during periods of
illness (“sick day rules”)
• Take insulin or oral hypoglycemic agents as usual.
• Test blood glucose and (for type 1 DM) test urine
ketones every 3 to 4 hours.
• Report elevated glucose levels (greater than 300
mg/dl) or urine ketones to the physician.
• Insulin-requiring patients may need supplemental
doses of regular every 3-4 hours.
• If usual meal plan cannot be followed, substitute
soft foods (e.g., 1/3 cup regular gelatin, 1 cup
cream soup, ½ cup custard, 3 squares graham
crackers) six to eight times per day.
Guidelines to follow during periods of
illness (“sick day rules”)
• If vomiting, diarrhea, or fever persists, take
liquids, (e,g., ½ cup regular cola or orange juice, ½
cup broth, 1 cup Gatorade) every ½ to 1 hour to
prevent dehydration & to provide calories.
• Report nausea, vomiting, & diarrhea to the
physician because extreme fluid loss may be
• For patients with type 1 diabetes, inability to
retain oral fluids may warrant hospitalization to
avoid diabetic ketoacidosis & possibly coma.
Hyperosmolar hyperglycemic
nonketotic state (HHNK)
Hyperosmolar hyperglycemic
nonketotic state (HHNK)
• HHNK is very similar to DKA in that it is a lifethreatening emergency caused by severe
hyperglycemia. It is clinically different from
DKA in that ketoacids are not formed and
acidosis is usually minimal.
• This is likely due to the patient producing
enough insulin to adequately prevent
• The typical HHNK patient is elderly with poorly
controlled or undiagnosed Type 2 diabetes.
• They often present with many symptoms which
mimic those of DKA, including:
• polydipsia,
• polyuria,
• weakness,
• weight loss,
• tachypnea (not Kussmaul respirations) and
• tachycardia
• Volume loss is significant in these patients due
to increased urination and electrolyte
imbalances, so look for signs of hypovolemia
and dehydration including dry mucous
membranes, orthostatic hypotension and
sunken eyes
• Volume loss is significant in these patients due
to increased urination and electrolyte
imbalances, so look for signs of hypovolemia
and dehydration including dry mucous
membranes, orthostatic hypotension and
sunken eyes
• Hypoglycemia is defined as a BGL of less than
80 mg/dl with symptoms consistent with a
diagnosis of hypoglycemia which resolve after
glucose administration.
• However symptoms usually don’t appear until
BGL are less than 60 mg/dl.
• If the patient is alert and oriented enough to maintain
their airway they can be given oral glucose 15g or an
alternative such as a drink with sugar added.
• If the patient is unable to obtain their own airway 1mg of
glucagon can be given intramuscularly or subcutaneously,
or establish an IV and administer 1g/ kg of a 50 percent
dextrose in water solution (D50).
• Due to the drug’s ability to cause thrombophlebitis, the
dose for pediatric patients is 1cc/kg of a 25 percent
solution, and a 10 percent solution is used in neonates. Of
course, all doses are dependent on the paramedic’s local
• When administering D50, the paramedic
should consider administering thiamine as
well, if it’s in their protocols.
• Any patient with a history of alcohol
intoxication or suspected malnourishment
could be thiamine deficient.
• Many patients treated for hypoglycemia are
well aware of their condition and will refuse
transport, and others will want to go for
physician evaluation.
• The paramedic should follow local protocol
on patient refusals. If no transport is required,
it is important that the patient eats a meal
containing complex carbohydrates, as glucose
is a simple sugar which is utilized quickly.
• Hyponatremia can be caused by salt-losing
states, such as
– vomiting or diarrhea,
– diuretic excess,
– adrenal insufficiency, or by excess total body water
states such as:
• the infection-induced syndrome of inappropriate
secretion of antidiuretic hormone (SIADH),
• nephrotic syndrome, and
• cirrhosis.
 Factitious, or pseudohyponatremia, can occur with
hyperglycemia, hyperlipidemia, or hyperproteinemia
In infants, hyponatremia is commonly due
to excess gastrointestinal loss from prolonged
vomiting or diarrhea, or from inappropriately
diluted formulas. Pyridoxine-dependent
seizures are a rare cause of intractable
seizures in neonates.
is typically defined as a serum sodium level
less than 125 to130 mEq/L, although clinical
symptoms are not usually seen until serum
sodium falls below 120 mEq/L.
 Manifestations include:
 altered mental status,
 vomiting,
 diarrhea,
seizures, and
 circulatory collapse.
• Treatment should be geared toward the
underlying cause. Aggressive treatment with 3%
hypertonic saline (514 mL/kg) should only be
initiated if significant symptoms are present, such
as seizures or coma.
• A dose of 1048 KWON & TSAI5 mL/kg over 10 to
15 minutes should raise the sodium level by
approximately 5 mEq/L; smaller additional doses
of 2 to 3 mL/kg can be considered if there is no
clinical improvement.
Hepatic Encephalopathy
Liver-largest internal organ in humans.
Portal Veins
• Vein that carries blood from the digestive
organs, gall bladder, & spleen, especially the
vein from the intestine carrying nutrient-rich
 synthesis of proteins, immune and clotting factors,
and oxygen and fat-carrying substances.
 Its chief digestive function is the secretion of bile, a
solution critical to fat emulsion and absorption.
 The liver also removes excess glucose from
circulation and stores it until it is needed.
 It converts excess amino acids into useful forms and
filters drugs and poisons from the bloodstream,
neutralizing them and excreting them in bile.
The liver has two main lobes, located just under the
diaphragm on the right side of the body. It can lose 75
percent of its tissue (to disease or surgery) without
ceasing to function.
Hepatocyte – liver cells
Sinusoid – small vessel in organ tissue
Shunt – divert channel
Varix or varices – swollen or knotted vein
Collateral – additional
Hepatic Encephalopathy
• Definition: Cerebral dysfunction associated
with severe liver disease.
• Pathophysiology:
– Inability of the liver to metabolize substances that
can be toxic to the brain such as ammonia, which
is produced by the breakdown of protein in the
intestinal tract.
Alcohol Abuse
Billiary Obstruction
Destruction of
Edema/ Ascites
Development of
collateral channels
Obstruction of blood flow
↑pressure in the venous and
sinusoidal channels
Fatty infiltration
shunting of blood
Increased pressure in
capillaries arteries
Shunting of ammonia &
toxins from intestine
into the general
Sign and Symptoms:
Lack of mental alertness to
Personality changes
Decerebrate rigidity
Liver cirrhosis
Medical Treatment
• Restriction or elimination of dietary protein
• Lactulose or neomycin to inhibit protein
breakdown, decrease bacterial ammonia
production, cleanse bowel of bacteria and
Nursing process
• 1. mental status, LOC: lethargy progressing to
– Dullness, slurred speech
– Behavioral changes, lack of interest in grooming or
• 2. Neurological exam: twitching, muscular
incoordination, asterixis (a flapping tremmor)
– arm-flapping caused by liver failure:
• a recurrent flapping tremor of the arms, like the action of a
bird's wings, that occurs as a result of a brain condition
associated with liver failure.
• 3. elevated serum ammonia level
Early signs of encephalopathy
• Restlessness
• Slurred speech
• Decreased attention span
To decrease ammonia production
• Reduce dietary protein to 20-40 g/day,
maintain adequate calories.
• Decrease ammonia formation in the intestine
– Give laxatives, enemas as ordered
– Administer lactulose (Cephulac) & neomycin (oral
or rectal) as ordered.
• presence in the bloodstream of too many
chemical wastes such as urea, a nitrogen-rich
waste product attributable to extra protein in the
– As chemical wastes build up in the body they produce
a toxic effect, possibly resulting in drowsiness,
irritability, nausea, vomiting, breathlessness,
headaches, and muscle cramps.
• In extreme cases, uremia may cause convulsions,
coma, or death.
Uremia most commonly develops
• when the kidneys fail to function properly.
• when blood flow to the kidneys is reduced
due to severe bleeding, serious burns, or
heart attack.
• when more wastes are formed in the
bloodstream as a result of traumatic injuries
or large surgical incisions.
• kidney stone, a tumor in the urinary tract, or a
severely enlarged prostate in males
• Victims of uremia due to kidney failure
undergo kidney dialysis, a medical procedure
that removes wastes from the blood.
• Transplantation of kidneys from healthy
donors to uremic patients has also proven
effective in some cases.