Hypoglycemia associated with the disequilibrium between dasg,
used in treating diabetes (insulin or tablets sahorosnizhayuschie
means), and eating or physical activity. A sharp drop in the concentration of glucose
leads to loss of consciousness, since the normal functioning of
brain depends almost entirely on glucose. Patients with diabetes can develop following
coma directly related and
specifically due to underlying disease, ketoatsidoticheskaya,
hyperosmolar and hypoglycemia.
speed and timeliness of providing care to patients in a comatose state in
largely determine the prognosis. Therefore, from this viewpoint the correct management of patients
prehospital seems to be most important.
hypoglycemia coma ranked third (5.4%) in the stascture of the complex on
prehospital and diabetes (3%), fifth (data NNPOSMP).
ketoatsidoticheskaya Diabetic coma
ketoatsidoticheskaya Diabetic coma (DKA), severe complications of diabetes mellitus
, characterized by metabolic acidosis (pH less than 7.35 or
bicarbonate concentration less than 15 mg / dL), increased anion gap,
hyperglycemia above 14 mmol / L, ketonemiey. Often develops in type 1 diabetes.
frequency from 5 to 20 cases per 1000 patients per year (2 / 100). Mortality 5-15%
for patients older than 60 years of 20%. From ketoatsidoticheskoy coma diesmorethan 16%
patients with type 1 diabetes. Cause of DKA absolute or pronounced
relative insulin deficiency due to inadequate insulin therapy or
increase in insulin requirements.
Aggravating factors:
Often, the etiology of DKA is still unknown. It should be remembered that up to 25% of cases
DKA seen in patients with newly diagnosed diabetes.
Clinical picture and classification
There are three stages of diabetic ketoacidosis (Table 1 ):
1. moderate ketoacidosis .
2. precoma or decompensated ketoacidosis .
3. Coma .
Complications ketoatsidoticheskoy coma, deep vein thrombosis, pulmonary embolism,
arterial thrombosis (myocardial infarction, cerebral infarction, necrosis), aspiration pneumonia
, cerebral edema, pulmonary edema, infection, rarely HMC and ischemic colitis,
erosive gastritis, late hypoglycemia. Indicated severe respiratory
failure, oliguria and renal failure. Complications of therapy edema
brain and lungs, hypoglycemia, hypokalemia, hyponatremia, hypophosphatemia.
Diagnostic criteria
1. Feature of the gradual development of DKA, usually over several days
.
2. Symptoms of ketoacidosis (the smell of acetone in exhaled air, breath
Kussmaul, nausea, vomiting, anorexia, abdominal pain).
3. The presence of symptoms of dehydration (decreased turgor of tissues, tone eye
apples, muscle tone, tendon reflexes, body temperature and blood pressure).
should remember that when type 2 diabetes should always seek
intercurrent disease as the cause of decompensation of diabetes mellitus.
list of questions obligatory for the diagnosis of DKA Prehospital:
whether the patient is suffering from diabetes?
whether there was a history of DKA?
whether a patient receives blood glucose-lowering therapy, which, the last taking the dasg?
when was the last meal or inadequate food intake or skip it?
whether there was too heavy physical exercise or alcohol intake?
which recently carried the disease was preceded by a coma (infectious diseases
)?
Was polyuria, polydipsia and weakness?
Possible errors therapy and diagnosis of pre-hospital:
1. Insulin prehospital without the possibility of determining the level of glycemia
and its control.
2. The emphasis in treatment on intensive insulin therapy in the absence of effective
rehydration.
3. Introduction to insufficient liquids.
4. The introduction of hypotonic solutions, particularly early in treatment. This may
lead to cerebral edema and intravascular hemolysis.
5. The use of forced diuresis rather than rehydration. The use of diuretics
simultaneously with the introduction of liquids only slow recovery
water balance, and when hyperosmolar coma appointment diuretics
categorically protivopakazano.
6. Initiation of therapy with the administration of sodium bicarbonate can lead to death
patient. Proved that an adequate insulin therapy in most cases
helps eliminate acidosis. Correction of acidosis with sodium bicarbonate involves
extremely high risk of complications. The introduction of alkali increases hypokalemia,
violates the dissociation of oxyhemoglobin, carbon dioxide, which forms the introduction
bicarbonate, increases intracellular acidosis (blood pH although there may
increase); paradoxical acidosis observed in the cerebrospinal fluid that
may contribute to brain edema, can not be asled Development rikoshetnogo "alkalosis.
rapid introduction of sodium bicarbonate (jet) can cause death from
rapid development of hypokalemia.
7. The introduction of sodium bicarbonate solution without introducing
preparations of potassium, which causes pronounced hypokalemia, which
becomes the cause of death of patients.
8. Cancel or fails to appoint insulin DKA patient who is unable to
eat.
9. Subcutaneous injections of insulin to patients in diabetic coma, which
absorption of insulin is violated due to microcirculatory disorders.
10. Intravenous jet administration of insulin. Half-life of insulin
intravenously 35 minutes, and only the first 15-20 minutes
concentration in the blood is maintained at a sufficient level, and so this route of administration
ineffective.
11. 34hkratnoe appointment of short-acting insulin (ICDs), subcutaneous (
in the early stages of DKA, when the state of moderate and no loss of consciousness,
possible appointment of insulin subcutaneously). The effective duration of action
ICD is 4-5 hours, especially in ketoacidosis. Therefore, the ICD should
name at least 5-6 times a day without night-break.
12. Application to deal with the collapse of simpatotonicheskih dasgs. They,
first, are kontrinsulinovymi hormones and, second, in diabetic patients
their stimulating effect on the secretion of glucagon is considerably stronger than
in healthy individuals.
13. Incorrect diagnosis of DKA. When DKA is not uncommon so-called
"diabetic psevdoperitonit" which simulates the symptoms of "acute abdomen"
tension and soreness of the abdominal wall, reduction or disappearance of peristaltic
noise sometimes increase seasm amylase. Simultaneous detection of leukocytosis
might lead to misdiagnosis and the patient falls into
infectious (intestinal infection) or surgical ("acute abdomen") offices.
In all cases of "acute abdomen" or dyspeptic symptoms in patients with diabetes mellitus
necessary to determine the glycemic and Re tonurii.
14. Metered blood glucose any patients who are unconscious
condition often leads to the formulation of erroneous diagnoses "violation
cerebral circulation," "coma of unknown etiology, while the patient is
acute diabetic decompensation exchange substances.
Therapy for Prehospital presented in Table 2.
hyperosmolar coma ketoatsidoticheskaya
hyperosmolar coma is characterized by severe ketoatsidoticheskaya
dehydration, significant hyperglycemia (often above 33 mmol / l),
hyperosmolarity (more than 340 mOsm / L), hypernatremia above 150 mg / dL,
distinguished by the absence of ketoacidosis (ketonuria maximum (+)). Often
develops in elderly patients with type 2 diabetes. Occurs 10 times less than the DFA.
characterized by a high mortality (15-60%). The reason for the development of hyperosmolar coma
relative insulin deficiency and factors, which are accompanied
dehydration.
Aggravating factors:
should be remembered that one-third of patients with hyperosmolar coma has
previous diagnosis of diabetes.
clinical picture
increases for several days or weeks, excessive thirst, polyuria ,
severe dehydration, hypotension, tachycardia, focal or generalized seizures
. If at ECU upset the function of the CNS and peripheral nervous system
proceed according to the type of gradual fading of consciousness
and oppression of tendon reflexes, the hyperosmolar coma accompanied
various mental and neurological disorders. Furthermore soporous
states are also often celebrated with hyperosmolar coma, mental disorders often occur
type of delirium, an acute hallucinatory psychosis,
katotonicheskogo syndrome. Neurological disorders occur
focal neurological symptoms (aphasia, hemiparesis, tetraparesis, polymorphic
sensory impairment, abnormal tendon reflexes, etc.).
Diagnostic criteria
1. Developsmoreslowly (within 5-14 days) than DKA.
More severe dehydration (decrease in turgor of tissues, the tone of the eyeballs,
muscle tone, tendon reflexes, body temperature and blood pressure).
2. Often polymorphic neurological symptoms, which disappears in relieving
hyperosmolar coma.
3. The absence of ketoacidosis (odor of acetone in exhaled air, no
breathing Kussmaul, nausea, vomiting, anorexia, abdominal pain).
4. The absence of ketonuria or unexpressed.
5. Previously, there anuria and azotemia.
6. Elderly age.
Among the possible errors in diagnosis and therapy are distinguished:
1. The introduction of hypotonic solutions on the prehospital stage.
2. Long-term introduction of hypotonic solutions.
3. Hyperosmolar syndrome is often mistakenly regarded as reactive
psychosis, cerebrovascular paroxysm or other acute mental or
neurological disease.
therapy is considered in Table 3.
hypoglycemia coma
hypoglycemia coma develops due to a sharp reduction in blood glucose
(below 33.5 mmol / l) and express the energy deficit in the brain
brain.
Aggravating factors:
overdose of insulin
omission or inadequate food intake
Increased physical activity
excessive alcohol intake
dosage ( b-blockers, salicylates,
sulfonamides, phenylbutazone, anabolic steroids, calcium supplements,
tetracycline, lithium carbonate, pyridoxine, inhibitors of MAO, clofibrate).
clinical picture
symptoms of hypoglycemia are divided into early (cold sweat, especially on forehead,
pale skin, strong attacks of hunger, trembling hands, irritability,
weakness, headache, dizziness, numbness of the lips), intermediate (
inappropriate behavior, aggressiveness, heart palpitations, poor coordination of movements, double vision
eyes, confusion) and late (loss of consciousness, convulsions).
Diagnostic criteria
1. The sudden development, usually for several minutes, less hours.
2. The presence of characteristic symptoms of hypoglycemia.
3. Glycemia below 3-3,5 mg / dL.
It should be remembered that the absence of symptoms does not asle out hypoglycemia and
patients with diabetes, symptoms of hypoglycemia may be at normal
concentration of glucose in the blood.
standard questions a doctor at the prehospital stage:
whether the patient suffers from diabetes, its duration;
receives a glucose-lowering therapy (which, last taking the dasg);
inadequate food intake or its omission, the last meal;
any episodes of hypoglycemia in the past;
too heavy physical exertion;
taking excessive amounts of alcohol.
should remember the most frequent cause of loss of consciousness in diabetes mellitus type 1
is severe hypoglycemia.
After removing the patient from hypoglycemic coma recommended
tools to improve the microcirculation and metabolism in the brain cells in
for 36 weeks. Recurrent hypoglycemia can lead to the defeat of
cerebral cortex.
possible errors of diagnosis and therapy:
1. The attempt to introduce carbohydrate foods (sugars, etc.) in the oral cavity
patient is unconscious. This often leads to aspiration and asphyxia.
2. Application for relief of hypoglycemia are not suitable for this product (bread,
chocolate, etc.). These products do not have enough action saharopovyshayuschim
or raise blood sugar, but too slowly.
3. Incorrect diagnosis of hypoglycemia. Part of the symptoms of hypoglycemia may
mimic an epileptic seizure, stroke, autonomic crises "and others have
patients receiving glucose-lowering therapy in almost any obscure
paroxysmal able to determine the appropriate extra blood sugar. When
no possibility of determining the level of glucose or the relatively slow
performing this analysis ekspresslaboratoriyami (30-40 min), when informed
suspected hypoglycemia its relief should begin immediately, even before receiving a response
laboratory.
4. Often do not address the risk of relapse after removal of heavy
hypoglycemia. With an overdose of insulin action and extended
sulfonylurea hypoglycemia may recur, and therefore the patient
requires intensive monitoring, control blood glucose levels and necessary?? Widely regarded as one of its
correction within a few days.
Therapy hypoglycemic coma is presented in Table 4.
Дифференциальнодиагностические criteria coma in DM
presented in Table 5.
Conclusion
patients who are in coma of unknown origin, always
necessary to investigate glycaemia. If you know for certain that the patient
diabetes and at the same time it is difficult to differentiate hypo or hyperglycaemic
genesis of a coma, we recommend intravenous
jet injection of glucose at a dose of 20-40-60 ml 40% solution in order to
differential diagnosis and emergency care during hypoglycemic coma
. In the case of hypoglycemia, it will significantly improve the symptoms and thus
to differentiate these two states. In the case of hyperglycemic coma
is the amount of glucose in the patient's condition is practically not affected.
In all cases it is impossible to measure blood glucose immediately empirically
need to introduce highly concentrated glucose. Estrenno uncropped
hypoglycemia can be fatal.
basic dasgs for patients in a coma with no possibility of
diagnosis and emergency hospital admissions are thiamine 100 mg IV, glucose
40% - 60 ml and 0.42 mg of naloxone IV. This combination is effective and safe in
many cases.
Published with permission from Russian
Medical Journal.