Acute complications of diabetes


• Hyperglycemic: 

– ketoacidotic;

– hyperosmolar non-ketoacidotic;

– lactic acidotic.

• Hypoglycemic. 

Diabetic ketoacidosis and ketoacidotic coma

The main reason is absolute or pronounced relative insulin-deficiency.

Provocative factors

• Intercurrent diseases: 

– acute inflammatory processes;

– exacerbation of chronic diseases;

– infectious diseases.

• Violations of the treatment regimen: 

– skipping or unauthorized withdrawal of insulin by patients (including those with suicidal goals);

– Errors in prescribing or administering a dose of insulin;

– the introduction of expired or improperly stored insulin;

• malfunction in insulin injection systems (syringe pens).

• Lack of control (and self-monitoring) of blood glucose levels. 

• Surgical interventions and injuries. • Pregnancy.

• Untimely diagnosis of diabetes, especially type 1.

• unassigned by insulin readings at long TEKU present type 2 diabetes.

• Chronic therapy with insulin antagonists (glucocorticoids, diuretics, sex hormones, etc.). 


Clinical picture• Increased dryness of the skin and mucous membranes • Polyuria (oliguria and anuria are possible later) • Thirst • Weakness, adynamia • Headache • Lack of appetite, nausea, vomiting • Drowsiness • Odor of acetone in exhaled air • Shortness of breath, subsequent Kussmaul breathing · • В 30 50% of cases are “abdominal syndrome,” that is, a clinic of “acute abdomen” (abdominal pain, frequent vomiting, tension and soreness of the abdominal wall, decreased peristalsis, leukocytosis and increased amylase activity are possible)  
Total kliniches cue blood test• Leukocytosis (does not always indicate an infection)
General urine analysis• Glucosuria • Ketonuria • Proteinuria (intermittent)
Blood chemistry• Hyperglycemia • Giperketonemiya • Increased BUN (impermanent) • Increased creatinine (impermanent; possible artefak you due to cross-reaction with ketone are Lamy with some laboratory methods) • Level Na + more normal, sometimes lowered or raised • Level of K + most normal, less often, in patients with renal failure may be increased
KShchS• Decompensated metabolic acidosis






At the prehospital stage or reception department:

– blood glucose analysis;

– urine analysis for acetone;

– short-acting insulin 20 units / m;

– 0.9% solution of sodium chloride in / drip at a rate of 1 l / hour.

In the intensive care unit or intensive care unit

Laboratory control:

– express analysis of blood glucose – 1 time per hour until glycemia decreases to 13-14 mmol / l, then 1 time in 3 hours;

– urine analysis for acetone (if possible, ketone bodies in serum) 2 times a day for the first 2 days, then 1 time per day;

– general analysis of blood and urine – initially, then 1 time in 2-3 days;

– sodium, potassium in plasma – 2 times a day;

– serum creatinine – initially, then 1 time in 3 days;

– gas analysis and the pH of capillary blood -1-2 times a day until the normalization of the acid base;

– hourly control of diuresis (permanent urinary catheter) until dehydration is eliminated or until consciousness is restored and urination is voluntary. 


– 0.9% sodium chloride solution (at a Na + plasma level <150 meq / l);

– 0.45% sodium chloride solution (hypotonic) (at the level of plasma Na + , we 150 meq / l);

– when glycemia below 14 mmol / l – 5-10% glucose solution (preferably but 10%), optionally together with nat. solution;

– colloidal plasma substitutes (in case of hypovolemia, systolic blood pressure below 80 mm Hg or central venous pressure below 4 mm Hg). 

Rehydration rate:

1st hour – 1000 ml nat. solution; 2nd and 3rd hour – 500 ml each. solution, pos leduyuschie hours – 300-500 ml saline. solution *

The rehydration rate is adjusted depending on the central venous pressure indicator or according to the rule: the volume of fluid introduced per hour can exceed the hourly diuresis by no more than 500-1000 ml. 

Insulin Therapy – Low Dose Regimen

At the 1st hour: 10-14 units of short-acting insulin iv in a jet.

Preparation of insulin solution for simultaneous intravenous administration (in the gum of the infusion system):

required number of units of short-acting insulin type syringe in insulinovyi and reach the 1 mL of 0.9% sodium chloride, & Input ditsya for 1 minute.

In the next clock (to reduce glucose to 14mmol / l) – insulin SHORT someone steps 4-8 units per hour (on average, 6 units per hour) on / in continuously via perfusors (infusomats) or 1 time per hour ” gum “infusion system

Preparation of insulin solution for perfusion:

50 units of short-acting insulin + 2 ml 20% human serum albumin to bring the total volume to 50 ml with 0.9% chlorite solution of sodium chloride.

Preparation of a solution for / drip insulin (at least before respectfully than the use or administration perfusors “vrezinku”:

per 100 ml of 0.9% sodium chloride – 10 units of insulin is short of action + 2 ml 20% human serum albumin (infusion with MSE growth of 40-80 ml per hour, which does not coincide with the fluid infusion rate to re-hydration and requires the installation of a separate I / O system).

In the absence of 20% human serum albumin , the adsorption of insulin on glass and plastic in the vial and infusion systems is from 10% to 50%, which makes it difficult to control and adjust the administered dose. Therefore, if it is not possible to use 20% human albumin, it is better to administer insulin into the gum of the infusion system, as described above.

If the glycemia level does not decrease 2-3 hours after the start of insulin therapy, double the dose of insulin in the next hour.

The rate of decrease in glycemia is not more than 5.5 mmol / l per hour and not lower than 13-14 mmol / l on the first day (with a more rapid decrease – the risk of osmotic imbalance syndrome and cerebral edema ).

With glycemia below 14 mmol / l – 3-4 units of short-acting iv insulin in the gum for every 20 g of glucose administered (200 ml of 10% or 400 ml of 5% glucose solution).

Intramuscular or subcutaneous administration of insulin is ineffective due to poor absorption (impaired microcirculation).

Intramuscular administration of insulin may be used in the impossibility NOSTA of intravenous insulin according to the following scheme:

• initial dose – 20 units of short-acting insulin / m;

• subsequent administration – 6 units of short-acting insulin 1 time per hour;

• after stabilization of glucose level at a level no higher than 10-12 mmol / l, the rate tion of KHS, recovery of consciousness and stabilizing blood pressure – translation hypodermis hydrochloric fractional therapy with short-acting insulin (every 4-5 hours for dose dependence of the glucose level) ; in addition to the short-acting insulin, a cart can administering background (prolonged insulin) at doses of 10-12 U 2 times a day from the first day after transfer to subcutaneous insulin therapy.

Recovery of electrolyte disturbances

Due to the high risk of rapid development of hypokalemia, iv drip of potassium preparations begins simultaneously with the start of insulin therapy at the rate of:

KS1 administration rate (grams per hour)
plasma(meq / l)at pH <7.1at pH> 7.1pH not included, rounded
> 6Potassium preparations to be administered

If the level of K plasma is unknown, intravenous drip of potassium preparations is started no later than 2 hours after the start of insulin therapy, under the supervision of an ECG and diuresis.

Metabolic Acidosis Correction

The etiological treatment of metabolic acidosis in ketoacidotic coma is insulin therapy.

Indications for the administration of sodium bicarbonate are strictly limited:

• blood pH less than 7.0 or standard bicarbonate level less than 5 mmol / l;

• Without determining pH / KHS, the routine administration of bicarbonate is contraindicated.

Nutrition of the patient after removal from a ketoacidotic coma

Once improvement of the patient, recovery of consciousness, spo lities swallow in the absence of nausea and vomiting shown fractional gentle power with a sufficient amount of carbohydrates, moderate to lichestvom proteins (porridge, mashed potatoes, bread, soup, scrambled eggs, did dennye juices without adding sugar) with an additional s / c administration of short-acting insulin at a dose of 4-8 units per meal. After 1-2 sous current after the start of the meal in the absence of disease exacerbation same ludochno-intestinal tract, the patient may be transferred to ordinary food.

Hypersmolar non-ketoacidotic coma

Main reasons

Expressed relative insulin deficiency + sharp degid Ratac.

Provocative factors

– Conditions causing dehydration: 

– vomiting, diarrhea (. Particularly common infectious diseases of punk Reate);

– the use of diuretics;

– violation of the concentration function of the kidneys;

– bleeding;

– burns;

– concomitant diabetes insipidus;

– incorrect medical advice (prohibition enough sweat Use by liquid when the thirst).

– Conditions enhancing insulin deficiency: 

– intercurrent diseases;

– surgical interventions and injuries;

– chronic insulin therapy antagonists (glucocorticoids on lovymi hormones, etc…); 

– therapy with somatostatin analogues (octreotide).

– old age 


Clinical picture• Marked dryness of the skin and mucous membranes • Marked polyuria (later oliguria and anuria are possible) • Marked thirst • Weakness, adynamia • Reduced skin turgor • Softness of the eyeballs on palpation • Drowsiness • There is no smell of acetone in exhaled breath • Kussmaul is absent polymorphic neurological symptoms (reche stems disorders, nystagmus, paresis, paralysis, convulsions, and so on. d.), often dominant in the clinical picture disappears after the removal of hyperosmolarity. It is extremely important differential diagnosis of swelling of the brain in order to avoid erroneous destination urine of chasing INSTEAD rehydration 
Blood chemistry• Severe hyperglycemia (usually above 30 mmol / l) • Lack of ketonemia • Normal levels of acid-base syndrome • Hypernatremia
Calculation of plasma osmolarityPlasma osmolarity (mosmol / l) = = 2 x (Na + meq / l + K + meq / l) + glucose (mmol / l) + + urea (mmol / l) + 0.03 x total protein (g / l )  Urea and total protein can be ignored (shortened formula)Norm: 285-300 msmol / l
Analysis of urine• Massive glucosuria • No acetonuria






In the intensive care unit or intensive care unit.


• at the level of Na +> 165 mEq / L administering saline solutions contraindicated but rehydration begins with 2% glucose solution;

• at the level of Na + 145-165 mEq / l of rehydration is accomplished 0.45% (hypotension cal) sodium chloride solution;

• when the Na + level decreases to <145 meq / L, rehydration is continued with a 0.9% sodium chloride solution.

Rehydration rate:

1st hour – 1000-1500 ml of physical solution; 2nd and 3rd hour – 500-1000 ml of physical. solution; the following hours – 250-500 ml of physical. solution *

The rehydration rate is adjusted depending on the central venous pressure index or according to the rule: the volume of fluid introduced per hour can exceed the hourly diuresis by no more than 500-1000 ml. 

Insulin therapy

It is carried out according to the same principles as with a diabetic ketoacidotic coma, but taking into account the high sensitivity to insulin in this type of coma, taking into account the following features.

At the start of the infusion therapy of insulin is not administered or is administered in ma mated doses (about 2 units of short-acting insulin in the h / w “in the gum” infu Zeon system).

If after 4-5 hours from the start of the infusion therapy, after partial re hydration and reduce Na + severe hyperglycemia persists, switching to insulin dosing regimen recommended for the treatment of diabetic coma ketoatsidoticheskaya.

With the simultaneous start of rehydration 0.45% (hypotonic) sol rum sodium chloride and erroneous administration of higher doses of insulin (6-8 units or more per hour) may dramatically rapid reduction of oc-molarity and create the osmotic gradient reverse developmental optionally ratim pulmonary edema and cerebral edema.

The optimal rate of decrease in osmolarity is not more than 10 mosmol / hour. Recovering Potassium Deficiency 

It is carried out according to the same principles as with a diabetic ketoacidotic coma.

Because of the potential concomitant development and ketoatsidoticheskaya giperos molar state laboratory control in both types of com conducts Xia equally, and the calculation of the plasma osmolarity is carried out in each case.

Lactic acid coma and lactic acidosis

Lactic acidosis classification

Associated with TKA Neva hypoxiaNot associated with tissue hypoxia
Type AType B1Type B2VZ type
Cardiogenic shockDramatically and permanently decompensated diabetes mellitusBiguanidesType 1 glycogenosis (Girke’s disease – G6PDH deficiency)
Endotoxic, hypovolemic shock, carbon monoxide poisoningImpaired renal or hepatic functionParenteral administration of fructose, sorbitol, xylitol in large quantitiesMethylmalonic Acidemia
AnemiaMalignant neoplasmsSalicylates 
PheochromocytomaHemoblastosisMethanol ethanol 
EpilepsyInfectious diseasesCyanides 

Provocative factors

• Increased production of lactate (reception biguanide expressed DEKOM pensation of diabetes mellitus, diabetic ketoacidosis, acidosis other genesis). 

• Reduction of lactate clearance (defeat liver parenchyma zloupot Use by alcohol). 

• Simultaneous decrease in clearance of lactate and biguanides (impaired renal function, intravenous administration of radiopaque agents). 

• Tissue hypoxia (chronic heart failure, coronary artery disease, obli-teriruyuschie peripheral arterial disease, severe disease op ganas respiration, anemia (folievo-, B12 and iron deficiency). 

• The combined effect of several factors leading to the accumulation of lactate (acute stress, expressed late complications of diabetes, age> 65 years, severe general condition, advanced stages of malignant but voobrazovany). 

• Pregnancy. Diagnostics 

Clinical picture• Persistent muscle pain that cannot be stopped by taking analgesics• Pain in the heart, not stopping taking antianginal drugs• Stomach ache• Weakness, adynamia• Headache• Nausea, vomiting• Arterial hypotension• Drowsiness, turning into a state of stupor, stupor and coma• Shortness of breath, subsequently breathing Kussmaul
Biochemical analysis of blood and KHS• Hyperlactatemia• Decompensated metabolic acidosis• “Anionic gap”: Na + – (СГ + НСОЗ ”)> 16 meq / L, and НСОЗ” <18 meq / L






In the intensive care unit or intensive care unit

Reduced lactate production

The introduction of short-acting insulin at 2-5 units per hour in / in the “gum” of the infusion system or using perfusion with a 5% glucose solution of 100-250 ml per hour.

Removal of excess lactate and biguanides (if used)

The only effective measure is hemodialysis.

Recovery of KShchS:

• artificial hyperventilation (mechanical ventilation) to eliminate excess CO2;

• introduction of alkali (sodium bicarbonate), with extreme caution, in ma mated doses (not exceeding 50 ml 8.5% sodium bicarbonate solution once) (risk of paradoxical enhance intracellular acidosis and increased lactate production).

The fight against shock and hypovolemia

For general principles of intensive therapy, using colloid GOVERNMENTAL plasma expanders and vasopressors.

Hypoglycemic coma and hypoglycemia

The main reason

• Excess insulin in the body in relation to the intake of carbohydrates from the outside (with food) or from endogenous sources (production of glucose by the liver), as well as with accelerated utilization of carbohydrates (muscle work).

Provocative factors

• Violation of the diet (skip timely meals or insufficient exact content of carbohydrates in it).

• An overdose of insulin or sulfonylurea preparations, including for suicidal purposes. 

• Drinking alcohol.

• Physical activity (unplanned or without the adoption of appropriate constituents of hypoglycemia prevention).

• Impaired liver and kidney function.

• The lack of carbohydrate for immediate kupirova Nia mild hypoglycemia.


Clinical picture• Adrenergic symptoms: tachycardia, mydriasis, trembling, pallor of the skin, increased sweating, nausea, severe hunger, anxiety, aggressiveness • Neuroglucopenic symptoms: weakness, impaired concentration, headache, dizziness, paresthesia, a sense of fear, disorientation; speech, visual, behavioral disorders, amnesia, impaired coordination of movements, confusion, coma; cramps passing into paresis and paralysis are possible.
Blood test• Glycemia below 2.8 mmol / L (with coma – usually below 2.2 mmol / L)


Mild hypoglycemia (without loss of consciousness and not requiring the assistance of another person)Receiving digestible (simple carbohydrates) in Included Quantity stve 1-2 HE: sugar (4-5 pieces dissolve better in water or tea), or honey, jam or (1-1.5 tablespoons) or 200 ml of sweet fruit juice, lemonade or 100 ml (Pepsi-cola, forfeits), or 4-5 large tablets glyu goats (pack of 10 tablets of 3 g as “Config thou”), or 2-4 chocolates.If hypoglycemia is caused by prolonged-acting insulin, then additionally eat 1-2 XE of slowly digestible carbohydrates (a piece of bread, 2 tablespoons of porridge, etc.).
Severe hypoglycemia (with or without loss of consciousness, but requiring the assistance of another person• Before the arrival of the doctor, the unconscious patient should be laid on his side, and the oral cavity should be free of food debris. If unconscious patient can not affect Vat in the mouth sweet solutions (risk ac CONST!) • V / a bolus of 40% glucose solution if honors from 20 to 100 ml, to full recovery of consciousness • Alternative – n / a or / m glucagon administration of 1 ml of solution (may be effected RELATIVES com patient) • in the absence of recovery of consciousness after i / v injection of 100 ml of 40% glucose solution – start I / drip administration 5-10% solution of glucose and transport the patient to the hospital • If hypoglycemic coma caused by re Oziri Coy oral hypoglycemic drugs with long duration of action, especially in elderly patients or concomitant yuschem impaired renal function, in / drip introduced Th 5-10% glucose solution can be continued huddle as long as necessary for the normalization of glycemia tion     

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