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
ketoacids.
• 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 &
glycerol.
• 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 METABOLIC ACIDOSIS.
 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 ketoacidosis

Insulin lack

↓Glucose utilization by the ↑Breakdown of fat

muscle, fat & liver

↑Fatty acids
↑Glucose production by
liver  Acetone
breath ↑ketone bodies
 Anorexia
Hyperglycemia  nausea

 n/v acidosis
Blurred vision polyuria  Abdominal
pain
 Weakness dehydration
 headache
↑respirations
polydipsia
 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
 Treatment
• Aimed at correction of the three main
problems:
– 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 dangerous.
• 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 life-

threatening 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
glyconeogenesis
• 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

• 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.
 Treatment
• 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
protocols.
• 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
• 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.
 Hyponatremia
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,
lethargy,
 vomiting,
 diarrhea,
seizures, and
 circulatory collapse.
 Treatment
• 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
food.
 Functions
 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.
 terminologies
• 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.
 Etiology:
Pathophysiology
·Alcohol Abuse
·Malnutrition
·Infection
·Drugs
·Billiary Obstruction Increased pressure in Portosystemic Splenomegaly
capillaries arteries shunting of blood

Destruction of Edema/ Ascites

HEPATOCYTES Anemia Leukopenia

Development of Shunting of ammonia &

collateral channels toxins from intestine
FIBROSIS/SCARRING
into the general
circulation
Caput Esophageal
medusae varices
Obstruction of blood flow Hepatic
↑pressure in the venous and Encephalopathy
sinusoidal channels
Fatty infiltration
FIBROSIS/SCARRING

Sign and Symptoms:

·Lack of mental alertness to
PORTAL confusion
HYPERTENSION ·Convulsion
·Asterexis
·Personality changes
·Decerebrate rigidity
·Coma
CAPUT MEDUSAE
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
protein.
Nursing process
 Assessment
• 1. mental status, LOC: lethargy progressing to coma.
– Dullness, slurred speech
– Behavioral changes, lack of interest in grooming or
appearance
• 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.
uremia
 Uremia
• presence in the bloodstream of too many chemical
wastes such as urea, a nitrogen-rich waste product
attributable to extra protein in the diet.
– 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.
Thanks…..