Download 05. Emergency care acute complications of diabetes mellitus

Acute complications of
diabetes mellitus: diagnostic
criteria and treatment
Classification of acute
complications of DM
Acute
complications of
DM
Hypeglycemic
comas
Nonketonic
hyperglycemichyperosmolar
syndrome (NKHHS)
Hypoglycemic
coma (HC)
Diabetic
ketoacidisis
(DKA)
Lactic
acidosis
(LA)
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Introduction
 Occur in both types of DM( type 1 and 2)
 Mortality rate in NKHHS is raging form 10~50%, depending on
underlying disease.
 Mortality rate in DKA is less than 5%.
 Thirteen medications and medication classes were implicated,
alone or in combination, in hospitalizations for adverse drug
events. The four most commonly implicated — warfarin
(33.3%), insulins (13.9%), oral antiplatelet agents (13.3%), and
oral hypoglycemic agents (10.7%) — accounted for an
estimated two thirds of hospitalizations
 An estimated 2–4% of deaths of people with type 1 diabetes
have been attributed to hypoglycemia
Pathogenesis of DKA
Type 1 diabetes
Initiating event
Insulin
Lypolisis
Glucagon
Protein catabolism
Glycerol
FFA´s
Amino acids
Ketogenesis
Hyperglicemia
Gluconeogenesis
Ketonuria
Osmotic
diuresis
Volumen depletion
Dehydration
Electrolite depletion
Acidosis
Ketonemia
Precipitating factors:
1)
2)
newly diagnosed diabetes (presenting manifestation);
inadequate administration of exogenous insulin (inadequate
dose, insulin infusion catheter blockage, mechanical failure
of insulin infusion pump);
3) increased requirements for insulin caused by the presence
of an underlying stressful condition:
•
an intercurrent infection (pneumonia, cholecyctitis);
•
a vascular disorder (myocardial infarction, stroke);
•
an endocrine disorder (hyperthyroidism,
pheochromocytoma);
•
trauma;
•
pregnancy;
•
surgery ;
•
medication (eg, corticosteroids, pentamidine, clozapine)
4) Idiopathic (no identifiable cause)
Clinical presentation
Diabetic ketosis.
It is status which is characterized by increased
level of ketones in blood, without clinical signs
of dehydration and can be corrected by diet (fat
restriction) and regular insulin injection.
DKA develops
over a period
of days or weeks.
Clinical presentation
nausea, vomiting
abdominal pain
palpitation
Signs and symptoms.
Laboratory findings
Investigations
1. A presumptive bedside diagnosis is justified if the
urine is strongly positive for both glucose
and ketones.
2. Measurement of blood ß-hydroxybutyrate (ß OHB) concentration, may not be available in all
labs, besides, urine Ketone testing can be
misleading due the following reasons:
•
◦ The used method does not detect the major
ketone body B-hydroxybutyrate. (sodium
nitroprusside only measures acetoacetate and
acetone). Serum ß-OHB concentrations, may be
increased to levels consistent with DKA when a
urine ketone test is negative or shows only trace
or small ketonuria
•
◦ The readings are qualitative depending on color
comparisons
•
◦ High doses of Vitamin C may cause falsenegative results, while some drugs may, on the
other hand, give false-positive results.
Diagnostic Criteria
PG mg/dl
Arterial pH
Serum HCO3
Urine Ketones
Serum
ketones
Effective SO
(mOsm/kg)
Anion gap
Mental status
Mild
>250
Moderate
>250
Severe
>250
7.25-7.3
15-18
7.0-7.24
10 -15
<7.00
<10
positive
positive
positive
positive
positive
positive
variable
variable
variable
>10
Alert
>12
alert/drowsy
>12
stupor/coma
Treatment
The goals of therapy include:
1. Reduction of hyperglycemia
2. Rehydratation
3. Correction of electrolyte imbalance
4. Correction of acid-base imbalance
5. Investigation of precipitating factors, treatment
of complications.
6. Frequent patient monitoring
Fig. Management of adult patients with DKA. 2003 American Diabetes Association.
©2003 by Canadian Medical Association
Chiasson J et al. CMAJ 2003;168:859-866
Nonketotic hyperglycemic-hyperosmolar
state (NKHHS or HNS).
HNS is a syndrome characterized by impaired
consciousness, sometimes accompanied by seizures,
extreme dehydration, , and extreme hyperglycemia
that is not accompanied by ketoacidosis.
The syndrome usually occurs in patients with type II DM,
who are treated with a diet or oral hypoglycemic
agents, sometimes it is a complication of previously
undiagnosed or medically neglected DM (type II).
HNC usually develops after a period of symptomatic
hyperglycemia in which fluid intake is inadequate to
prevent extreme dehydration from the hyperglycemiainduced osmotic diuresis.
Predisposing factors
1.
2.
3.
•
•
•
5.
6.
7.
HNS seems to occur spontaneously in about 5 – 7 % of patients.
Infection (e.g., pneumonia, urinary tract infection, gram-negative
sepsis) is underlying frequent precipitating cause.
Use of certain drugs has been associated with this condition:
steroids increase glucogenesis and antagonize the action of
insulin;
potassium-wasting diuretics (hypokalemia decreases insulin
secretion), e.g., thiazides, furosemide;
other drugs, e.g., propranolol, azathioprine, diazoxide.
Other medical conditions such as cerebrovascular accident,
subdural hematoma, acute pancreatitis, and severe burns have
been associated with HNS.
Use of concentrated glucose solutions, such as used in
peripheral hyperalimentation or renal dialysis, has been
associated with HNC.
HNS can be induced by peritoneal or hemodialysis, tube
feeding.
Clinical presentation
1. Polyuria, polydipsia, weight loss, weakness and
progressive changes in state of consciousness from
mental cloudiness to coma (present in 50 % of
patients) occur over a number of days to weeks.
2. Because other underlying conditions (such as
cerebrovascular accident and subdural hematoma)
can coexist, other causes of coma should be kept in
mind, especially in the elderly.
3. Seizures occur in 5 % of patients and may be either
focal or generalized.
Physical examination
1. Severe dehydration is invariably present.
2. Various neurologic deficits (such as coma, transient
hemiparesis, hyperreflexia, and generalized
areflexia) are commonly present. Altered states of
consciousness from lethargy to coma are observed.
3. Findings associated with coexisting medical
problems (e.g., renal disease, cardiovascular
disease) may be evident.
Laboratory findings
Laboratory findings
•
Diagnosis and treatment of diabetic ketoacidosis and the
hyperglycemic hyperosmolar state. CMAJ April 1, 2003 vol. 168 no.
7 859-866
Laboratory findings
Treatment
This condition is a medical emergency and the patient
should be placed in an intensive care unit.
Many of the management techniques recommended
for a patient with DKA are applicable here as well.
The goals of therapy include:
•
•
•
•
rehydration;
reduction of hyperglycemia;
electrolytes replacement;
investigation of precipitating factors, treatment of
complications.
Diabetes Care January 2004 vol. 27 no. suppl 1
s94-s102
Lactic acidosis (LA)
DM is one of the major causes of LA, a serious condition
characterized by excessive accumulation of lactic acid
and metabolic acidosis.
The hallmark of LA is the presence of tissue hypoxemia,
which leads to enhanced anaerobic glycolysis and to
increased lactic acid formation.
The normal blood lactic acid concentration is 1mmol/l,
and the pyruvic to lactic ratio is 10:1. An increase in
lactic acid without concomitant rise in pyruvate leads
to LA of clinical importance.
Pathogenesis
Predisposing
factors
1. Heart and pulmonary failure (which leads to
hypoxia).
2. Usage of bigyanids.
3. Alcohol intoxication.
4. Ketoacidosis (it is important to have a very
high index of suspection with respect to
presence of LA).
Metformin-Associated Lactic Acidosis
• Incidence:
0.03 cases/1,000 patient-years
•
Mortality:
about 50% of cases
• Sign and symptoms:
non-specific (nausea, vomiting, altered consciousness,
fatigue, abdominal pain, and thirst)
1.Gowardman JR. Fatal metformin induced lactic acidosis: case report. N Z Med J 1995;108:230-11.
2.Gan SC, Barr J, Arieff AI, Pearl RG. Biguanide-associated lactic acidosis.
Case report and review of the literature. Arch Intern Med 1992;152:2333-6.
3.Bailey CJ, Turner RC. Metformin. N Engl J Med 1996;334:574-9.
4.Lee AJ. Metformin in noninsulin-dependent diabetes mellitus. Pharmacotherapy 1996;16:327-51.
Clinical presentation
Physical examination
1.
2.
3.
4.
5.
6.
Acrocyanosis is common.
Tachycardia frequently is present, blood pressure
is decreased.
Poor skin tugor and dry skin may be prominent.
Hypothermia is common in LA.
Hyperpnea or Kussmaul respiration are present
and related to degree of acidosis.
Findings associated with coexisting medical
problems (e.g., renal disease, cardiovascular
disease) may be evident.
Laboratory findings
1.
2.
3.
Blood glucose level is not high
Glucosurea is absent.
Blood lactic acid is high.
Treatment of LA
LA is treated by correcting the underlying cause.
Oxygentherapy
Metylen blue (50 – 100 ml of 1 % solution i/v droply)
Sodium bicarbonate therapy should be used
LA can be treated with low dose insulin regimens with 5 %
glucose solution infusion.
Symptomatic therapy:
- Hydrocortisone (250 mg i/v)
- Unitiol (5% solution 10 ml i/v (1- 2 ml/10 kg)
- α-lipoid acid (tioctic acid)
- thiamine (its deficiency may be associated with
cardiovascular compromise and lactic acidosis. The
response to thiamine repletion (given as 50-100 mg
intravenously [IV] followed by 50 mg/d orally [PO] for 1-2
wk) may be dramatic and potentially lifesaving).
Sodium bicarbonate
• The starting dose of sodium bicarbonate (NaHCO3-) is
one third to one half of the calculated extracellular
bicarbonate (HCO3-) deficit, as illustrated by the
following formula:
HCO3 deficit (in mEq) = 0.5 × (Wt in kg) × (Desired
HCO3 – Measured HCO3)
• Metabolic alkalosis can ensue after bicarbonate
administration if the correction is complete rather than
partial. This result can be avoided by titration of the
bicarbonate dose to modest therapeutic end points
(eg, arterial pH of 7.20).
• Because of increased CO2 production, sodium
bicarbonate may precipitate ventilatory failure and, as
such, must be given with caution.
Comparison of DCA, HNC and LA.
Hypoglycemia
It is a syndrome characterized by
symptoms of sympathetic nervous system
stimulation or central nervous system
dysfunction that are provoked by an
abnormally low plasma glucose level.
Hypoglycemia represents insulin excess
and it can occur at any time.
Causes:
1. complication of treatment of diabetes mellitus
with insulin or oral medications,
2. excessive insulin produced in the body
(hyperinsulinemia),
3. inborn error of metabolism,
4. medications and poisons,
5. alcohol,
6. hormone deficiencies,
7. prolonged starvation,
8. alterations of metabolism associated with
infection, and organ failure.
Risk factors for hypoglycemia
in diabetes (ADA, 2009)
www.uspharmacist.com: Cryer PE, Axelrod L, Grossman AB, et al. Evaluation and
management of adult hypoglycemic disorders: an Endocrine Society Clinical Practice
Guideline. J Clin Endocrinol Metab. 2009;94:709-728.
Patophysiology
Clinical presentation
1. adrenergic symptoms
(they are attributed to
increased sympathetic
activity and epinephrine
release):
- sweating,
- nervousness,
- faintness,
- palpitation
- sometimes hunger;
2. cerebral nervous system
manifestations: confusion,
inappropriate behavior
(which can be mistaken for
inebriation); visual
disturbances, stupor, coma
or seizures. (Improvement in
the cerebral nervous system
manifestations will be with a
rise in blood glucose.)
A common symptom of
hypoglycemia is the early
morning headache, which is
usually present when the
patient awakes.
Patients should be familiar with
the symptoms of the
hypoglycemia but some of
them are not heralded by
symptoms.
Physical examination
1. The skin is cold, moist.
2. Hyperreflexia can be elicited.
3. Hypoglycemic coma is commonly
associated with abnormally low body
temperature
4. Patient may be unconsciousness.
Laboratory findings
1. Low level of blood glucose
• It is suggested that persons with diabetes
become concerned about the possibility of
developing hypoglycemia when the selfmonitored blood glucose concentration is falling
rapidly or is no greater than 70 mg/dl (3.9
mmol/liter) (An Endocrine Society Clinical
Practice Guideline, 2009)
Treatment
Insulin–treated patients are advised
to carry sugar lumps, candy, or glucose tablets
at all time.
Asymptomatic or mild-to moderate symptomatic
hypoglycemia are effectively self-treated by ingestion of
glucose tablets or carbohydrate-containing juice, soft
drinks, milk, candy, other snacks, or a meal. Patients
have to teach their family members to give such
treatment if they suddenly exhibit confusion or
inappropriate behavior.
• A commonly recommended dose of glucose in adults is
20 g. Clinical improvement should occur in 15–20 min.
Treatment
• Parenteral treatment is necessary when a hypoglycemic
patient is unwilling (because of neuroglycopenia) or unable
to take carbohydrate orally.
• Glucagon 1.0 mg in adults by an associate of the patient s/c,
i/m. Although glucagon can be administered iv by medical
personnel, in that setting the standard parenteral therapy is
iv glucose. If the patient does not respond to 1 unit of
glucagon within 25 minutes, further injections are unlikely to
be effective, and are not recommended;
Treatment
• A standard initial glucose dose is
25 g. The glycemic response to iv
glucose is, of course, transient.
• an i/v injection of 20 or 100 ml of
40-50 % glucose, followed by a
continuous infusion of 5 %
glucose (10 % glucose may be
needed) until it clearly can be
stopped safely;
• Food should be provided orally as soon as the patient
is able to ingest it safely.
• glucocorticoids and adrenaline are helpful as well.
• Octreotide has been used to treat sulfonylureainduced hypoglycemia
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