Acute complications of diabetes mellitus : etiology ...



Acute complications of diabetes mellitus :

etiology, pathogenesis, diagnostic criteria, treatment

One of the most important tasks for a practice doctor is diagnosis and treatment of urgent states. The large diseases group, which might complicated with acute painful state and require urgent medical treatment, are diseases of endocrine system, and first of all – the diabetes mellitus, which is one of the leader in spreading of diseases structure. Therefore, only the knowledge of clinic symptomatology, diagnostic questions, differential diagnosis and treatment of an urgent state allows the doctor to render the appropriate and qualified treatment for patient.

Diabetes mellitus (DM) is a systemic disease that effects essentially every organ of the body. The fatal outcome is related to the development of acute or chronic complications.

Classification of acute complications of DM.

1. Diabetic coma:

1) diabetic ketoacidisis (DKA);

2) nonketonic hyperglycemic-hyperosmolar coma (NKHHC);

3) lactoacidosis (LA).

2. Hypoglycemic coma (HC).

At present there are three kinds of diabetic comas: ketoacidic, hyperosmic and lactacidemic. The medical tactics depends on the pathogenic of diabetic coma, therefore a pathogenic disease diagnosis has a special meaning. Yet to take into account that a diabetic ketoacidosis, hyperosmotic and hyperlactacidemical syndromes are rarer as a pure form. Usually two or even three pathogenic varieties in different combinations (including over the expressiveness degree of any syndrome) are appearing from the expressive diabetes decompensation beginning moment.

Diabetic ketoacidisis (DKA).

Before the area of insulin therapy, ketosis was the leading cause of death of patients with DM. Since insulin deficiency worsens the clinical picture and leads to metabolic abnormalities, the complication is more common in young diabetics. Despite insulin usage, mortality remains high (6 - 10 %).

DKA results from grossly deficient insulin modulation of glucose and lipid metabolism. A diabetes ketoacidic coma is one of the most dangerous complications and appears as a result of the growing insulin deficiency. The diabetic ketoacidosis development (DKA) is the more typical for IDDM. But it must be remembered that patient with IDDM may have DKA in cause of the present of stress situations and intercurrent diseases which lead to decompensation of diabetes mellitus.

Precipitating factors:

1) newly diagnosed diabetes (presenting manifestation);

2) inadequate administration of exogenous insulin;

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.

Predisposing factors of DKA development.

1. Unrecognized diabetes mellitus.

2. Treatment regime violation (an absence of accurate insulin doses correction).

3. Infections and intoxication’s.

4. Physical, psychological trauma.

5. Surgical operations.

6. Acute cardiovascular insufficiency, myocardial infarction, cerebral hemorrhage.

7. Pregnancy.

8. Prolonged starvation.

9. The considerable change of diet, using of alcohol.

10. Insulinresistance (antibodies formation or isolation and destruction of insulin during subcutaneous injection).

11. Physical exercises (loading) during a chronic insulin deficiency.

Physical exercises may lead to the early and delayed hypoglycemia’s, increasing the glucose utilization and causing the more faster insulin absorption, which isn’t balanced with the liver increasing glucose production and supplementary food. There is less known the ability of physical exercises to cause ketoacidosis of those patients, who do not fully chronically receive insulin. Physical load stimulates a production of contrinsular hormones: adrenaline, STH, glucagon. These hormones mobilize glucose and fat and direct a metabolism in liver to the formation of ketones that may rapidly lead to the ketoacidosis during considerable insulin deficiency.

In the base of diabetic ketoacidosis and coma pathogenesis is the increasing insulin deficiency and as a consequence:

1. The infringement of glucose utilization with tissues, cytolemme hypopermeability for glucose, decreasing of processes of its oxidation and energetic using by cell.

2. The infringement of glycogen synthesis, at first of all in liver, that with combination with lipocain deficiency, leads to the fatty infiltration of liver.

3. Increasing of the glycogen dissociation, the compensative formation of glucose of proteins and fats (gluconeogenesis).

4. Hyperproduction of contrinsular hormones which having fatty - mobilized property: somatotrophin, catecholamines, and corticotrophin.

5. Hyperproduction of the basic hormonal antagonist – glucagon which promotes to the glucose production increasing.

6. Lipolysis increasing.

At present a ketoacidic coma is very severe complication of diabetes mellitus which is life – threatening for patient. During DKA mortality is 5-17%.

DKA develops then when insulin deficiency is combined with increasing activity of contrinsular hormones. Their effect (except STH) is showed very rapidly.

Glucagon increases hepatic glycogenosis and gluconeogenesis, during DKA its level increases on 400-500%. At increases the hepatic ketogenesis on 300%, independently on level of free fatty acids and also increases the lipolysis.

The catecholamines excretion is stimulated with activation of the sympathic nerval system, stress, acidosis, fever. The adrenaline level increasing stimulated glycogenolysis in liver and muscules, increases gluconeogenesis in liver, activates the lipase of fatty acids and secondary ketogenesis in liver. During insulin deficiency the increasing of blood CA leads to increasing of the glucose level in 5-7 ones higher then in normal.

The long increased STH level (acromegalia) leads to increasing production of glucose in liver, increases the lipolysis and ketogenesis.

Hyperglycemia causes osmotic diuresis and leads to dehydration, decreasing of electrolytes level and serum hypertony.

Patients, who are using the according to thirst liquid volume and having normal function of kidneys, have a moderately increasing of glycemia level during ketoacidosis, as in normal the kidneys may excreate glucose with the speed which is adequative to the increasing of glucose production.

Patients with vomiting or are in unconscious state can’t use enough liquid to level continuous osmotic diuresis which leads to dehydration and hypovolemia with decreasing of renal function.

It explains that fact only rehydration with solutions without insulin introducing, may to decrease the glucose level in half. The hospitalized patients with DKA have the loss of free water which is usually 10-15% (100-150 ml/kg of body weight) and depends on expressiveness and duration of disease. The hyperglycemia value presents about a dehydration and hypovolemia degree.

Hypovolemia makes more hardly the metabolic acidosis owing to two ways: the decreasing of tissue circulation and development of lactacidical acidosis, which may be 25% of acidemia during DKA. Also hypovolemia decreases the renal function and excreation of organic acids.

The osmotic diuresis during DKA leads to the passive electrolytes and water loss: Na – 5-13 m eq/kg, K – 4-10 m eq/kg, P – 0,5-4 m eq/l.

Every 100mg% (5,5 mmole/l) of the glycemia increasing decreases the sodium level in blood serum on 1,6 m eq/l.

Na = Na (measured) + 1,6 (glucose – 100)/100

Acidosis and catabolism of proteins stimulates the potassium excretion from cells. With urine the potassium is lossed because of increasing activity of aldosterone, stimulated with dehydration. During rehydration and insulin treatment may appears the hypokalemia (decreasing of serum hypertony, increasing of SHT, acidosis decreasing and potassium entering into a cell).

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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.

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Signs and symptoms.

1. Polydipsia, polyuria and weakness are the most common presenting complaints.

2. Anorexia, nausea, vomiting, and abdominal pain may be present and mimic an abdominal emergency.

3. Ileus and gastric dilatation may occur and predispose to aspiration.

4. Kussmaul breathing (deep, sighing respiration) is present as respiratory compensation for the metabolic acidosis and is obvious when the pH is less than 7.2.

5. Symptoms of central-nervous-system involvement include headaches, drowsiness, lassitude, stupor and coma (only 10 % patients are unconscious).

Physical examination.

1. Hypothermia is common in DKA. A fever should be taken as strong evidence of infection.

2. Hyperpnea or Kussmaul respiration are present and related to degree of acidosis, acetone may be detected on the breath (musty (fruity) odor to the breath).

3. Tachycardia frequently is present, but blood pressure is usually normal unless profound dehydration is present.

4. Poor skin tugor may be prominent depending on the degree of hydration.

5. Hyporeflexia (associated with low serum potassium) can be elicited.

6. Signs consistent with a “surgical abdomen” but which follow severe ketonemia can confuse the clinical picture.

7. In extreme cases of DKA one can see hypotonia, stupor, coma, incoordination of ocular movements, fied dilated pupils, and finally death.

8. Other signs from a precipitating illness can be present.

Laboratory findings.

1. The hallmark of DKA is the finding of:

- hyperglycemia;

- ketonemia;

- metabolic acidosis (plasma pH and bicarbonates are decreased.

2. A presumptive bedside diagnosis is justified if the urine is strongly positive for both glucose and ketones.

3. [pic]

4. Different changes of electrolyte levels in the blood can be observed and does not reflect the actual total body deficits.

5. Serum amylase and transaminases can be elevated.

6. Leucocytosis occurs frequently in DKA and therefore cannot be used as a sole indication of infectious process.

Types of DKA:

- abdominal;

- vascular collapse;

- cerebral (encephalopathic);

- renal;

- mixed.

Differential diagnosis.

DKA must be distinguished from a variety of clinical conditions, particularly those in which central-nervous system function is altered and also associated with metabolic acidosis. The patients history and physical examination often are adequate diagnostic techniques.

Cardiac arrhythmia is the severest complication of the potassium homeostasis infringement. The DKA development in according with the modern data may be represented with following stages:

I stage of ketoacidosis ( DKAI ).

Pathogenesis. This stage is characterized with growing hyperglycemia, which is a result of insulin deficiency. At that time on the base increasing of sugar level in blood, cells face energetic starvation, as a deficiency doesn’t give possibility for cells to utilize the glucose.

The energetic cellular starvation of organism leads to activation of the endogenic glucose formation owing to the gluconeogenesis and glycogenes dissociation. These processes are stimulated with glucagon, catecholamines, glucocorticoids. But the glucose utilization by cells in this situation isn’t arranged of insulin deficiency, and a result of this the hyperglycemia is increased some more. Hyperglycemia is accompanied with the increasing of osmotic pressure of blood serum, cellular dehydration, polyuria, glucosuria (glucose begins to exreat in urine of the glycemia level is 10-11 mmole/l). Glucosuria causes the increasing of osmotic pressure of primary urine, that prevent it from reabsorbtion and intenities polyuria.

The compulsory factor of DKA pathogenesis is an activation of the ketonal bodies formation. The insulin deficiency and surplus of contrinsular hormones (in first of all – the somatotrophic having lipolytic effect) lead to the lipolysis activation and free fatty acids (FFA) contains increasing, which are the ketogenic substrate. Exept these, the synthesis of ketonic bodies – beta-oximalar and acetoacetic is owing to “ketogenic” aminoacids (isoleucine, leucine, valine), which are accumulated as a result of proteins catabolism in causes of insulin deficiency. The ketonical bodies accumulation leads to exhaustion of alkaline blood reserves and development of metabolitic acidosis. In first stage of DKA there is appearing the moderate acetonuria which may be inconstant.

Clinics. DKA, as a rule, develops slowly, during some days, on the diabetes mellitus decompensation base. During this stage there is the decreasing or loss of efficiency, muscular debility, appetite disappearance. There is appearing of headache, dispeptic effects (nausea, diarrhea). The polyuria and polydipsia grow. During an examination there are revealed dryness of skin, tongue and mucousal membrane of oral cavity, feeble oral smell of acetone, muscular hypotony, tachycardia, some dull cardiac tones, possibly the arrhythmia. Sometimes there is pain in abdomen, it may be palpated the painful and increasing liver.

Laboratory data. Hyperglycemia until 18-20 mmole/l, glucosuria, ketonemia (untill 5,2 mmole/l) and ketonuria (ketonic bodies in urine – some positive). The aqueous electrolitic balance on this stage of DKA development is characterized with some hyperkaliemia (owing to the potassium excreation from cell) – until – 5 mmole/l. The potassium deficiency in cell is confirmed with ECG data (asymmetric decreasing of ST interval, the double – phasic T-wave, which may be negative). The acidic-alkaline state (AAS) doesn’t essentially change, but there is decreased the hydrocarbonaties contains until 19-20 mmole/l.

Treatment. Patients with diabetes mellitus on the first stage of DKA must be hospitalized into the endocrinal hospital department. There is important measure on this stage to change the diet regime. It is necessary to recommend easy-digested carbohydrates, fruit saps, honey. The common carbohydrates volume is increased until 70-75% for ketogenesis suppression. The hyperglycemia correction is because of the insulin of early effect, with small doses, not rarer than 6 ones per day (intramuscular). The insulin day doses is counted up owing to the 0,7-1,0 UN/kg of the factic body weight. For acidosis removal are prescribed the alkaline mineral waters (“Borzhomy”), dimephosphone, regidron. Are necessary also a cleansing enemas with 3% solution of sodium hydrocarbonate. As a rule, these measures are sufficiently for treatment of patients with DKA I stage. In case of the dehydration expressive signs to prescribe the intravenous solutions injection.

It must be noted that carly diagnosis and opportune treatment promote to prevention of the ketoacidosis beginning stage passing to the precoma which is vitally dangerous for patient.

Precomatous state (DKA II nd)

Pathogenesis. Following are the pathogenetic mechanisms: energetic cellular incompetence in causes of insulin deficiency is accompanied with activation of protein destruction which is leading to infringement of the nitrogen balance and promotes the azotemia development. It causes the increasing of endogenic glucose production from glycogene, fat and protein, is growing the glucosuria and polyuria owing to the osmotic diuresis. At first a glucosuria and hyperglycemia lead to cellular dehydration and then to general dehydration with decreasing of tissue and renal circulation and mineral deficiency (Na,K,Cl). The renal blood circulation infringement promotes to the ketoacidosis growing, because of kidney stopping the hydrocarbonic ion production (HCO3). Activation of ketoacidosis is increased with the metabolitic acidosis, which is accompanied with decreasing of the blood alkalinity and pH shifting. Stimulation of the respiratory center with hydrogen ions leads to the appearance of characteristic harsh infrequent breathing. Besides, as a result of the lipolysis activation in blood are accumulated FFA, non-etherificated fatty acids, tryglycerides, which increase blood viscosity and promote to infringement of hemorrhological blood properties and microcirculation insufficiency.

Clinics. On the DKA-II the general condition of patient is acute, deteriorated, rapidly grow thirst and polyuria. Patient is suffering of the progressive muscular debility and can’t individually move. It appears the pernicious vomiting and increased abdominal pain. There are often heart pains. During examination there are expressive xerodermia and xeromucous, rubeosis of face (as a result of capillary paresis). Tongue is dry, crimson or coated with brown fur, there is sharp fowl smell of acetone. Muscular tonus is decreased, the eyeboll tonus is decreased, too. Breathing begins infrequent, deep, harsh (Kussmaul respiration). From the side of cardiovascular system there are the following changes: rapid and soft pulse, tachycardia, dull heart sounds, may be the arterial hypertony. Hypokaliemia leads to the intestine motopity decreasing. As a result of intestine atony beginning it is strained off with its contents which is leading to appearance of painful syndrome. Except these, there is the tension of anterior abdominal wall. These changes may be a cause for false diagnosis of the “acute abdomen”. We must take into account that DKA is accompanied with leukocytosis with neutrophilia and formula shifting to the left (owing to hydrovolemia). Therefore the clinics of “acute abdomen”, that is confirmed with laboratory data, is seemed highly convincing. The result of this may be inexcusive laparatomy which making DKA tendency worse.

A peculiarities of the preceding diabetes mellitus tendency, patient age, accompanied diseases, Also as a causes character, which directly cause the acidosis, define the rapidness of its tendency, expressiveness and preclaiming in clinics that or other manifestations.

Due to these there are several forms of the precomatous state tendency.

Gastrointestinal (abdominal): there are spasmodic pains in epigastral and iliac regions acquiring then spilling character and seem on peritonitis, the defending tension of abdominal muscles, the restricting of this region during breathing (“acute abdominal” syndrome). Moreover, There are characterized by uncontrollable vomiting and vomitory reflexes with exceation of mucousal or mucous – bilious contents, which often acquiring the “coffee-ground” color (manifestations of the erosive toxic gastritis). Stools disturbances have enough steady and permanent character: persistent constipation’s are interchanged with profuse fetorical diarrheas with painful tenesmuses.

The causes of the hardlest abdomenalgia and pseudoperitonitis until present aren’t standed finally. One supposes that they are connected with stimulation of nodes of celiac plexus owing to the peritoneum vessels spasm. Others investigators assume those in causes of ketoacidic dehydration is developing the aseptic peritonitis. Some authors explain that pain is caused with spastical state of pylorus and intestine.

In some causes the painful sensations are connected with stretching of stomach owing to the toxic gastritis and transudation into its cavity of many liquid.

Abdominal pain caused with ketoacidosis lasts during 4-5 hours from the beginning of treatment. Often this form is found in young age.

Cardiovascular form: More oftenly it manifestetes in older age. The mean clinic manifestation is heavy collapse with considerable decreasing of arterial and venous pressure, tachycardia, weak pulse, different disturbances of cardiac rhythm, cyanosis and cold extremities. The cardiac asthma manifestations and sometimes the acute edema of lungs remind the clinic of acute myocardium infarction meeting during prolonged and hard tendency of diabetes mellitus.

In this form pathogenesis the cause is hypovolemia with considerable decreasing of blood circulated volume, decreasing of the contractive myocardial function in connection with atherosclerosis of coronal arteries and acute metabolic cardiomyopathy (hypokaliemia, acidosis, failure of miocardial energetic guarantee and soon), and also the peripheric vascular paresis. During this coma form the most frequent are developing thrombosises of pulmonary vessles, vessles of lower extremities and coronal vessles (with formation of transmural myocardial infarction).

Cardiovascular disturbances which accompanied with diabetic ketoacidotic coma may be called as a syndrome of acute circular insufficiency, of combined nature (cardiogenic, hypovolemic and metabolic hypocirculatory syndromes). For ketoacidotic coma is characteric a easy hypothermy, therefore the body temperature increasing in this condition on present of the infectional – inflammatory process.

Hypothermy promotes to development of the insulin-resistance, therefore during uncomplicated with infection coma it is necessary to use measures for patient warming.

Renal (nephrotic) ketoacidosis form is developing, as a rule, when the diabetes mellitus exists 20-30 years and during this period was more of less an expressive permanent urinary syndrome (albuminuria, microhematuria, constantly lower urinous concentration). In some causes manifestations of the Kimmelstiel-Wilson syndrome acquire a threatening character with progressively increasing uremia, anuria and general edema.

We can point out on a renal ketoacidosis variety, then decreasing of arterial systemic pressure and renal circulation lead to anuria and all of following clinical disease tendency is defended with acute renal insufficiency.

Encephalopathic (pseudocerebral) form is found in old people who suffer of the cerebral atherosclerosis. During ketoacidosis due to the hypovolemia, cellular dehydration, acidosis, microcirculation infringement is falling decompensation of chronic cerebrovascular insufficiency. It showes with symptoms of local lesions of brain: hemiparesis, assymmetry of reflexes, appearance of one-sided pyramidal signs. In this situation often is difficult to defind – either coma cause this focal symptomatology or insult be comes an cause of ketoacidosis.

The treatment that is beginning in time as ketoacidosis is removed leads to improvement of cerebral circulation and decreased of cerebral symptomatology.

Dehydrative form is observed in the middle and old age. Often a people with asthmatic constitution are suffering of this form, for them for the diabetes mellitus compensation in necessary many insulin (a day dose is about 100 units). Skin is coarse, rough, locally cracking, with grey-mat colour, skin fold doesn’t fall flat, an features are acute, ocular cavities are deep, eyelids are closed on half (mummification of face).

Even patient still in conciousness dosn’t co not contact with surrounded people owing to significant dryness of mucous membranes of mouth, throat, tongue and expressive asthemia. Chest is flat, intercostal spaces are deep and intensivly take part during breathing, abdomen is drawing in with very expressive the upper flaring portions of the iliums.

Laboratory data: on the precoma stuge the glycemia achieves 20-30 mmole/l and is accompanied with expressive polyuria and increasing plasma osmatic pressure untill 320 mo sm/l, it is significantly infringes the water-mineral balance which is showed with hyponatremia (loss 130 mmole/l), hypokaliemia (loss 4 mmole/l). For this stage of DKA are characteric evident infringements of AAS (the blood alkulinity is decreased 40 volume % and loss, HCO3 untill 10-12 mmole/l, pH from 7,35 to 7,10). The protein catabolism (owing to gluconeogenesis) is accompanied with increasing of the urea and creatinine levers in blood, proteinuria. It must be remembered that the urinary syndrome and nitrical compounds accumulation patients who have an diabetic nephropahty.

If on precomatous state to patient isn’t rendered any treatment then during 2-3 hours is developing the ketoacidic coma (DKA III rd).

DKA – III rd. Pathogenesis. The progressive dehydration leads to hypovolemia which is accompaning with blood circulation decreasing in kidneys and brain. An ketoacidosis progress intensifies hypoxia. It is increasing deficiency of the sodium, chlorides and espesially potassium.

Hypovolemia, hypoxia and potassium deficiency in principal define the comatous condition tendency. One of the hypoxia pathogenesis factors is an intestive increasing of concentration of glycosylated hemoglobin (Hb A1 and Hb A1C) which doesn’t transport an oxygen. Hypovolemia leads to development of the circulatory hypoxia. The infringanment of mineral balance is accompanied with myopathy, also with respiratory muscules debility that leads to applying of alveolar hypoxia compound. For hypoxia progress is assisting the activation of an anaerobic glycolysis and lactic acid accumulation in tissues.

These factors (hypovolemia, hypokaliemia, hypoxia and increasing of lactic acid level) promote to development (on the ketoacidosis base) cardiovascular insufficiency and metabolic coagulopathy.

Coagulopathy is showed as a disseminated intravascular coagulatis (DIC-syndrome), peripheric thrombosis and thromboembolisms. As a rule, hypovolemia is accompanied with renal perfusion infringement.

During incorrect and mistaked therapy, as already was mentioned, the ketoacidosis manifestations transfer into precoma and then into ketoacidotic coma.

There a 4 stades:

I. Stunning (patient is inhabited, consciousness in confused).

II. Somnolentia (patient sleeping, but cann’t independently answer the question).

III. Sopor (patient is in condition of deep sleep and may to wake up only under the powerful stimulations action).

IV. Coma (complete loss of consciousness).

Clinic. Patient face is pale, without cyanosis signs, sometimes there is a facial rubeosis. Skin is dry, cold, its turgor is decreased. Breathing begins deep and harsh, the inhalation phase is longed than exhalation (a large Kussmaul respiration). There is an acute smell of acetone from oral cowity, which may be noticed on enter of premises, where a patient is lying. During palpation eyeballs are soft owing to decreasing of the ocular muscles tonus.

Muscular tonus of extremities is decreased. Enough oftenly there are different changes of cardiovascular system (rapid and weak pulse, extrasystoles and ciliary arrhythmia), there is the expressive arterial hypotony.

Tongue is dry, with mal fur, abdomen is some distended. During palpation there is increased liver. Body temperature is decreased (except if there aren’t accompanied infectional – inflammatory processes).

Uresis is intentional, may be oligo- or anuria.

Pathogenesis of consciousness derangements and other psychoneurological symptoms of the ketoacidic coma isn’t understanded complete. During different time these derangements were connected by authors with following factors:

1) toxic affection on brain with ketonic bodies surplus;

2) cerebrospinal fluid acidosis (and possibly owing to intracellular acidosis of CNS);

3) cerebral cellular dehydration;

4) hyperosmotic pressure of intracellular space in CNS.

The most confirmed are two last factors. A sufficient proof of this is circumstance that the consciousness derangement and neurologic symptoms are expressive during hyperosmotic coma and considerably less during ketoacidosis.

Laboratory data. As a rule, glycemia on the ketoacidic coma stage is more than 30 mmole/l which is accompanied with increasing of plasma osmolarity untill 350 mosm/l and more other. Besides, on this stage of DKA is increasing the potassium sodium and chlorids deficiency and hyperazotemia. AAS is characterized with progressived acidosis (pH a decreases untill 7,1 and lower), abruptly decreases the reserve alklinity (30 %) and hydrocarbonatis level of blood. The lactic acid level is increasing untill 1,6 mmole/l and more other.

Treatment of the precomatous condition and ketoacidic coma.

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If a patient has diabetes mellitus with precomatous condition development, it is necessary special hospitalization into the emergency department where immediately begins the intensive therapy which consists of following compounds:

a) insulintherapy;

b) rehydration;

c) mineral balance correction;

d) acidic-alkaline state recovery;

e) correction of cardiovascular derangements;

f) elimination of factors which causing ketoacidosis.

The goals of therapy include:

1. Rehydratation.

2. Reduction of hyperglycemia.

3. Correction of: a) acid-base and b) electrolyte imbalance.

4. Investigation of precipitating factors, treatment of complications.

The most important factor to emphasize is the frequent monitoring of the patient both clinically and chemically. Initially, laboratory data should be obtained every 1 – 3 hours and less frequently once clinical improvement is noted. If the patient is in shock, stupor or coma, a nasogastric tube, especially if vomiting, and urinary catheter are recommended.

Frequent assessment of potassium status is vital. A lead II electrocardiogram (ECG) can be provide a rapid assessment of hyperkalemia (peaked T waves) and hypokalemia (flat T waves and presence of U waves). Hyporeflexia and ileus are clinical indications of potassium deficiency.

Careful observation of neurological status is vital to detect the infrequent but devastating presence of cerebral edema.

Rehydration.

The average fluid deficit in adults with DKA is 3 to 5 l. A rapid infusion of 0,9 % sodium chloride (e.g., 1 l/h for the first 1 to 2 hours) is given and then reduced to about 0,5 – 0,3 l/h if the blood pressure is stable and the urine follow is adequate. After the initial infusion, intravenous fluid therapy must be adjusted individually on the basis of urine output, clinical assessments of hydration and circulation, determination of plasma electrolytes and glucose. When serum glucose level is about 11 – 13 mmoll/l administration of 5 % glucose with insulin can be performed (1 to 2 unites of insulin on each 100 ml of 5 % glucose solution). The addition of glucose to the intravenous solution is necessary for correction of tissue lipolysis and acidosis.

Insulin treatment.

DKA can be treated with low dose insulin regimens; e.g., initial intravenous administration of 10 to 20 units of regular insulin followed by continuous intravenous infusion of 0,1 unit/kg/hour in 0,9 % sodium chloride infusion. (50 units of insulin can be added to a 500 ml bottle of 0,9 % sodium chloride solution to give 1 insulin unite/10 ml of solution.)

If the glucose level does not improve after an hour of infusion, the rate of insulin is doubled until a response is noted. But if there is a tendency for decreasing the level of glucemia we have to decrease the dose of insulin in two times.

When the serum glucose concentration reaches 11-13 mmoll/l, insulin can be given subcutaneously (if plasma and urine persistently negative for ketones). Blood glucose level should be maintained at about 11 mmoll/l during intravenous therapy.

Improvement usually is noted in 8 – 24 hours. Following stabilization of the clinical condition, patients are placed in insulin regimen consisting of five injections of regular insulin.

Treatment of electrolyte disorders.

As a rule, potassium should never be given until the state of renal function is known and until the serum potassium concentration is available. In most patients the initial serum potassium is high-normal or elevated, and the initiation of K replacement (20 to 40 mmoll/h) usually can be deferred for 2 hours, using hourly serum measurements as a guide.

Potassium would be to infuse at a rate of ml of 1,5 g/h during 3 – 5 hours.

Correction of metabolic acidosis.

The metabolic acidosis occurs due to insulin deficiency and dehydration. So ketone bodies are themselves metabolized to bicarbonate once proper therapy is begun (fluids, electrolytes, insulin) and exogenous administration of bicarbonate can overcorrect to alkalosis.

The use of bicarbonate can be recommended only in the following cases:

- if life-threatening hyperkalemia;

- when severe lactic acidosis complicates DKA;

- with severe acidosis (pH ................
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